Understanding and Treating Alzheimer’s

U.S. Food and Drug Administration (FDA) Acting Commissioner Dr. Janet Woodcock is calling on the Office of Inspector General (OIG) to carry out an investigation into the FDA’s approval of Biogen’s new Alzheimer’s drug, Aduhelm. 

Woodcock said in a letter posted to Twitter on Friday that she has "tremendous confidence in the integrity of the staff and leadership" in the FDA's Center for Drug Evaluation and Research. However, she agreed that there "continue to be concerns raised...regarding contacts between representatives from Biogen and FDA during the review process, including some that may have occurred outside of the formal correspondence process.

“To the extent these concerns could undermine the public’s confidence in FDA’s decision, I believe it is critical that the events at issue be reviewed by an independent body such as the Office of Inspector General in order to determine whether any interactions that occurred between Biogen and FDA review staff were inconsistent with FDA policies and procedures,” she wrote. 

Controversial approval

The FDA’s approval of Aduhelm sparked controversy because the agency’s advisory panel of experts didn’t believe there was enough evidence that the drug is effective at treating Alzheimer’s. Three members of the advisory panel resigned in protest following the FDA’s decision to approve the drug.

Biogen’s decision to set the drug’s list price at $56,000 per year has also been controversial. The approval and pricing of Aduhelm is being investigated by two Congressional House committees.

The OIG confirmed that it received Woodcock’s letter, but agency officials said they haven’t finished reviewing it, and they also haven’t decided whether to launch an investigation. In a statement, a Biogen spokesperson said the company will cooperate with any investigations.

House Representative Katie Porter (D-Calif.) released an open letter on Tuesday calling for the inspector general of Health and Human Services to take a deeper dive into the relationship between the U.S. Food and Drug Administration (FDA) and Biogen, the makers of a new drug for Alzheimer’s. 

In June, the FDA approved Biogen’s drug (now marketed as Aduhelm) by using an “accelerated” approval process similar to the consideration it gave COVID-19 vaccines that received emergency use authorization last year. 

The FDA said it uses the expedited approval process for treatments of a serious or life-threatening illness if the treatment in question is expected to be better than the options currently available to patients. 

The agency cited trials showing that the drug reduced amyloid plaque, which builds up in the brain and is believed to play a key role in causing Alzheimer’s disease. However, trials of the drug were paused in 2019 because they failed to show promising results. The following year, the FDA called together an expert panel to review the trial evidence of Adhulem. None of the experts involved recommended approving the drug, although one expert voted uncertain. 

Approval sparks debate

The agency's speedy approval of the antibody-based drug gave way to controversy. Three members of the FDA’s advisory panel resigned in protest, and at least one member questioned whether there is enough evidence to show that the drug is effective at treating Alzheimer’s disease.

Now, Porter wants officials to investigate the relationship between Biogen and the FDA. In the letter, Porter said it appears “very clear” that the drug maker “had an inside route to FDA officials and had undue influence over their decision making and the evidence presented in various settings.” 

“Patients should have confidence that their treatment plans are based on science, not cozy relationships between Big Pharma and FDA officials,” Porter said in a tweet. 

Porter is calling for “a full review” of the FDA’s communications with pharma executives, lobbyists, and other stakeholders. She is also calling on the agency to establish new policies that prevent “fraud, waste, and abuse.”  

Backlash regarding approval and pricing

Other lawmakers have also challenged the approval of the Alzheimer’s drug. In a letter to the Senate Finance Committee late last month, Sens. Elizabeth Warren (D-Mass.) and Bill Cassidy (R-LA) called for a hearing to “examine the vexing new questions and challenges” that Aduhelm presents to the Medicare program.

Separately, Sen. Joe Manchin (D-WV) urged President Biden in a letter last month to remove interim commissioner Dr. Janet Woodcock. He cited the FDA’s Aduhelm approval as his reasoning. 

Biogen’s decision to set the drug’s list price at $56,000 per year has also been controversial, but the drugmaker said recently that the estimated price is subject to change. The company said it won’t have to charge as much for the drug if demand turns out to be high. 

When the U.S. Food and Drug Administration (FDA) approved Biogen’s new Alzheimer’s drug Aduhelm last month, there was controversy over how the drug was approved and how it was priced. Now, the drugmaker says that the $56,000 a year estimated price is not exactly set in stone.

“We have determined the launch price of Aduhelm based on our belief in the impact of treatment as well as the size of the appropriate patient population based on the entry criteria of our clinical trials,” the company said in a statement. “In the event that our fundamental assumptions on population size and rate of adoption are significantly different than expected, we stand ready to work with public and private payers to address pricing in order to achieve both patient access and support budget sustainability.”

In other words, Biogen said it won’t have to charge as much if there is a higher demand for the drug. But the statement stopped short of suggesting what kind of price break the company might provide.

“We have been engaging directly with public and private payers and health systems to ensure coverage policies support access for appropriate patients,” the company said. “For example, we have already announced our intention to enter into innovative access agreements with Cigna Corporation and the Veterans Health Administration. We believe these will serve to stimulate further discussions with other payers on creating solutions to ensure access.”

Impact on Medicare’s budget

Biogen said it is also committed to engaging with the Centers for Medicare and Medicaid Services (CMS) on “innovative price and access agreements.”

Some of the pushback to Aduhelm has centered on concern about the cost to the government’s healthcare services. In a new report, the Kaiser Family Foundation concluded that the new drug has huge implications for Medicare’s budget since so many patients will want the drug.

“Alzheimer’s disease is estimated to affect about 6 million Americans, the vast majority of whom are age 65 and older and therefore eligible for Medicare,” the authors write. “As an intravenous infused medication administered by physicians, Aduhelm will be covered under Medicare Part B, which generally covers FDA-approved physician-administered medications that are reasonable and necessary for the individual patient.”

The report also concluded that it would cost taxpayers more than $57 billion if 1 million Medicare patients were to receive the drug. That’s more than what the program spends on all other drugs combined. 

Doubts about efficacy

The drug has also drawn fire for the way in which the FDA approved it. Three members of the FBA advisory panel that cleared the medication have resigned in protest, with at least one questioning whether the drug even works.

Memos released this week show that FDA staff members objected to the approval of the drug, arguing there was insufficient evidence that it was effective at treating Alzheimer’s disease.

An adviser to the FDA has resigned over the agency’s speedy approval of a new Alzheimer’s drug. 

Earlier this week, the agency approved aducanumab, which goes by the generic name Aduhelm, for the treatment of Alzheimer’s disease. The FDA used an “accelerated” approval process, similar to the consideration it gave COVID-19 vaccines that received emergency use authorization last year. 

The expedited process drew concern from critics who said it received far less consideration than other drugs do before they’re brought to market. 

Mayo Clinic neurologist Dr. David Knopman, a member of the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee (PCNS), resigned from the committee in protest of the drug’s approval. In a Wednesday interview with CNN, he said he and the other external advisers decided there wasn’t enough evidence to support approving the drug and disagreed with the FDA’s decision to do so. 

"I resigned from the PCNS committee because if I ever were asked to serve on a future panel, I wouldn't have wanted to be treated in the disrespectful way that the aducanumab external advisers were treated," he said. "While I disagree with the decision to approve aducanumab, we in the clinical care and clinical research worlds will simply have to learn to adapt to the new circumstances."

Advisory committee uncertain

Aduhelm, which is given by infusion, is the first new drug to be approved to treat Alzheimer’s in nearly two decades. It was approved for use in patients with “mild cognitive impairment,” which often signifies that the patient is on the path to dementia.

Trials of the drug were paused in 2019 over a lack of promising results. However, Biogen -- the company that makes the drug -- took another look at the data last year. The company said the data showed that some patients who got high doses of the drug hadn’t improved, but they had shown a slower rate of decline than other patients. 

In November, the PCNS committee convened and voted against the suggestion that it could help patients. The panel decided they were “uncertain” about whether the drug had any effects on the brain. The FDA isn’t required to make decisions that are in line with the advice of its committees, but it usually does. That’s why the decision to approve the drug raised eyebrows. 

The FDA said this week that patients who received the treatment had a significant reduction of amyloid beta plaque, while patients in the control portion of the initial trials had no reduction of amyloid beta plaque. Critics of the drug’s approval say Biogen may have been motivated by money to get the drug approved, given that the drug would be priced at $56,000 a year.

The U.S. Food and Drug Administration (FDA) has approved Aduhelm, whose generic name is aducanumab, for the treatment of Alzheimer’s disease. But the action is not without controversy.

The agency approved the drug using “accelerated” approval, similar to the consideration it gave the coronavirus (COVID-19) vaccines that received emergency use authorization (EUA) last year.

The FDA said the accelerated approval pathway can be used for a drug for a serious or life-threatening illness that provides “a meaningful therapeutic advantage over existing treatments.”

The drug is intended to reduce amyloid plaque, a substance in the brain that has been associated with Alzheimer’s. Scientists tested the drug in three separate studies representing a total of 3,482 patients. The studies consisted of double-blind, randomized, placebo-controlled dose-ranging studies in patients with Alzheimer’s disease. 

The FDA said patients receiving the treatment had a significant reduction of amyloid beta plaque but patients in the control arm of the studies had no reduction of amyloid beta plaque.

‘Victory for people living with Alzheimer’s’

“This approval is a victory for people living with Alzheimer’s and their families,” said Harry Johns, CEO of the Alzheimer’s Association. “This is the first FDA-approved drug that delays decline due to Alzheimer’s disease. This means individuals may have more time to actively participate in daily life, have sustained independence, and hold on to memories longer.”

The drug is produced by Biogen and Eisai, Co., Ltd., a Japanese biopharma firm. Biogen CEO Michel Vounatsos called the FDA approval “a historic moment.”

“We believe this first-in-class medicine will transform the treatment of people living with Alzheimer’s disease and spark continuous innovation in the years to come,” Vounatsos said. “We are grateful for the contributions of thousands of patients and caregivers who participated in our clinical trials, as well as for the dedication of our scientists and researchers. 

Critics’ concerns

The accelerated path Adihelm followed to its FDA approval has drawn concern from some critics who noted that it is an abrupt departure from how other drugs are brought to the market. The nonprofit group Public Citizen was particularly scathing in its rebuke.

“The FDA’s decision shows a stunning disregard for science and eviscerates the agency’s standards for approving new drugs,” said Dr. Michael Carome, director of Public Citizen’s Health Research Group. “Because of this reckless action, the agency’s credibility has been irreparably damaged.”

In addition, some doctors interviewed by the Wall Street Journal cautioned that the drug won’t be effective for every Alzheimer’s patient.

It will also be an expensive medicine. Biogen said that the typical patient would pay about $56,000 a year before insurance coverage for treatment with the drug. Cigna has estimated eligible patients may face $10,000 a year in out-of-pocket costs.

In 2021, the Alzheimer’s Association estimates about 6 million Americans are living with Alzheimer’s disease, which is a progressive cognitive illness for which there is no cure.

A new study conducted by researchers from the Medical College of Georgia suggests that cannabidiol, or CBD, may be beneficial to those at risk of developing familial Alzheimer’s. 

According to their findings, CBD was effective in improving cognitive abilities in mice with familial Alzheimer’s by restoring the function of two proteins in the brain that are compromised by the degenerative condition. 

“Right now we have two classes of drugs to treat Alzheimer’s,” said researcher Dr. John Morgan. “But we have nothing that gets to the pathophysiology of the disease.” 

The benefits of CBD 

The researchers conducted a study on mice to determine how CBD can benefit those struggling with familial Alzheimer’s. The mice were injected with CBD every other day for two weeks, and the researchers observed their brain function to see how the supplement affected Alzheimer’s progression. 

From a chemical perspective, CBD played a key role in regulating two proteins in the brain -- IL-33 and TREM2. TREM2 works to keep the organ clear of potentially harmful proteins like beta-amyloid, which is closely associated with Alzheimer’s. Similarly, IL-33 works to send signals throughout the brain when levels of proteins like beta-amyloid get too high. 

Prior to the CBD treatment, levels of both IL-33 and TREM2 were low, which is common for those with Alzhiemer’s. However, they found that those levels increased once they exposed the mice to CBD. 

The CBD was also effective at improving the mice’s overall cognitive function. The researchers assessed cognition by testing the mice’s ability to recognize objects familiar to them, and the results improved significantly following the CBD intervention. 

Blood pressure readings are always changing. Recent studies have found that different parts of the body -- like our arms -- can come back with very different numbers. While these changes are often normal and expected, a new study is exploring how certain blood pressure fluctuations could be a sign of more serious health concerns. 

According to researchers from Uppsala University, consumers with higher blood pressure at night could be at an increased risk of Alzheimer’s disease. 

“The night is a critical period for brain health,” said researcher Christian Benedict. “For example, in animals, it has previously been shown that the brain clears out waste products during sleep, and that this clearance is compromised by abnormal blood pressure patterns. Since the night also represents a critical time window for human brain health, we examined whether too high blood pressure at night, as seen in reverse dipping, is associated with a higher dementia risk in older men.” 

Normal versus abnormal blood pressure changes

To better understand how changes in blood pressure could affect Alzheimer's risk, the researchers had 1,000 men in their early seventies participate in the study. For more than two decades, the researchers observed the men’s health records and paid particular attention to fluctuations in blood pressure readings and cognitive health outcomes.

The researchers learned that the risk of Alzheimer’s was higher for participants who experienced higher blood pressure at night. While it’s normal for blood pressure to ebb and flow throughout the day, nighttime hours are typically when blood pressure is the lowest. In a healthy body, blood pressure can be as much as 20 percent lower at night than it is during the day. 

However, the opposite trend was observed in this study. Many of the men experienced spikes in their blood pressure at night, which experts refer to as “reverse dipping.” This trend was then linked with an increased risk of Alzheimer’s disease. 

“The risk of getting a dementia diagnosis was 1.64 times higher among men with reverse dipping compared to those with normal dipping,” said researcher Xiao Tan. “Reverse dipping mainly increased the risk of Alzheimer’s disease, the most common form of dementia.” 

The researchers plan to do more work based on these findings, including examining whether taking blood pressure medication at night can alleviate some concerns about cognitive decline. They also want to see whether older women are at a similar risk of Alzheimer’s based on changes in blood pressure.

Eli Lilly has provided a ray of hope for an aging population worried about the scourge of Alzheimer’s disease.

The pharmaceutical company has reported that its experimental Alzheimer’s drug donanemab helped Alzheimer’s patients in a small clinical trial. In the trial, the drug slowed the decline in memory and ability to perform activities by nearly one-third after 18 months.

The company said the drug met the main goal of the study, getting farther in the process than other Alzheimer’s drugs have.

“We are extremely pleased about these positive findings for donanemab as a potential therapy for people living with Alzheimer's disease, the only leading cause of death without a treatment that slows disease progression,” said Dr. Mark Mintun, vice president of pain and neurodegeneration at Eli Lilly.

Mintun said the positive results give hope for patients and their families. However, there have been previous promising findings in Alzheimer’s research that have failed to pan out.

Targets beta amyloid in the brain

Donanemab works by targeting N3pG beta amyloid in the brain, which is believed to be a major contributor to the cognitive decline caused by Alzheimer’s disease. The company says patients treated with donanemab instead of the placebo showed an 84 centiloid reduction of amyloid plaque at 76 weeks compared to a baseline of 108 centiloids.

In the study, patients stopped receiving donanemab and switched to a placebo once their plaque level was below 25 centiloids for two consecutive measures or below 11 centiloids at any one measure.

"This unique mechanism and antibody for clearing plaques, discovered at Lilly, has the potential to provide high levels of durable amyloid plaque clearance after limited duration dosing," said Dr. Daniel Skovronsky, Lilly's chief scientific officer and president of Lilly Research Laboratories. 

Skovronsky said Lily researchers hoped to determine if reducing amyloid plaques in Alzheimer's patients to levels seen in scans of healthy individuals could result in a clinically meaningful slowing of cognitive decline. In that regard, he said the test was successful.

Slowly developing disease

Alzheimer's disease is a type of dementia that affects memory, thinking, and behavior. Symptoms may grow slowly, but they eventually become severe enough to interfere with daily tasks.

Alzheimer's is a degenerative disease that worsens over time. In its early stages, memory loss is mild, but with late-stage Alzheimer's, individuals lose the ability to carry on a conversation and function in daily life. 

Alzheimer's is the sixth-leading cause of death in the United States, according to the Alzheimer’s Association.

Air pollution continues to be a concern for consumers’ health around the world, and recent studies have shown the ways that young people’s physical and mental health are negatively affected by these toxins. 

Now, a new study conducted by researchers from Lancaster University has found that exposure to polluted air can increase the risk of young people developing serious neurological conditions, including Parkinson’s, Alzheimer’s, and motor neuron disease (MND). 

“It’s critical to understand the links between the nanoparticles you’re breathing in or swallowing and the impacts those metal-rich particles are then having on the different parts of the brain,” said researcher Barbara Maher. “Different people will have different levels of vulnerability to such particulate exposure but our new findings indicate that what air pollutants you are exposed to, what you are inhaling and swallowing, are really significant in development of neurological damage.” 

Neurological risks

The researchers scanned the brainstems of 186 participants from Mexico City to see what effect lifelong exposure to contaminated air can have on neurological health.

The researchers observed noticeable changes to two parts of the participants’ brains: the cerebellum and the substantia nigra; the former is responsible for overall body movement while the latter is the source of dopamine production. The researchers say these parts of the brain were sites for nanoparticles related to exposure to air pollution.

The researchers explained that these nanoparticles increase the likelihood of inflammation throughout the brain and can also lead to abnormalities in protein levels, all of which can increase the likelihood of Parkinson’s, Alzheimer’s, and MND. 

“Not only did the brainstems of the young people in the study show the ‘neuropathological hallmarks’ of Alzheimer’s, Parkinson’s, and MND, they also had high concentrations of iron-, aluminum-, and titanium-rich nanoparticles in the brainstem -- specifically in the substantia nigra, and cerebellum,” said Maher. 

“The iron- and aluminum-rich nanoparticles found in the brainstem are strikingly similar to those which occur as combustion- and friction-derived particles in air pollution (from engines and braking systems,” she continued. “The titanium-rich particles in the brain were different -- distinctively needle-like in shape; similar particles were observed in the nerve cells of the gut wall, suggesting these particles reach the brain after being swallowed and moving from the gut into the nerve cells which connect the brainstem with the digestive system.” 

The researchers only examined participants between the ages of 11 months and 27 years old, but their findings showed that there were already signs of neurological degeneration. The team worries about how negative health effects will manifest over time and hopes that efforts will be taken to better control air pollution. 

While researchers have found ways consumers can protect themselves against Alzheimer’s disease, a new study is exploring how certain medications can increase the risk of cognitive decline.

According to researchers from the University of California at San Diego, anticholinergic drugs, which are used to treat everything from high blood pressure to allergies, can put consumers at an increased risk of Alzheimer’s disease. 

“This study...suggests that reducing anticholinergic drug use before cognitive problems may be important for preventing future negative effects on memory and thinking skills, especially for people at greater risk for Alzheimer’s disease,” said researcher Lisa Delano-Wood, PhD. 

Knowing the risks

The researchers had nearly 700 participants involved in the study, none of whom were exhibiting any signs of memory or cognitive struggles when the study began. Participants reported on the anticholinergic drugs they were taking, which can be administered as either over-the-counter or prescription drugs, and the researchers assessed their health outcomes over the course of a decade. 

The researchers learned that not only were the participants taking nearly five different types of anticholinergic drugs, but the doses of the drugs were much higher than what is typically recommended -- especially for older people. Taking these drugs in such high quantities was linked to memory and cognitive impairments as the study progressed. 

The researchers also looked at the participants’ genetic make-up to determine how the combination of any pre-existing factors and the presence of anticholinergic drugs could affect the likelihood of participants developing Alzheimer’s. Ultimately, the researchers also identified a link there, as cognitive impairments were 2.5 times more likely when participants were taking anticholinergic drugs and presented with existing risk factors. 

While the researchers plan to do more work in this area moving forward, they hope that these findings show how anticholinergic drugs can be a detriment to consumers’ cognitive function as they age. 

“This points to a potential area for improvement since reducing anticholinergic drug dosages may possibly delay cognitive decline,” said researcher Alexandra Weigand. “It’s important for older adults who take anticholinergic medications to regularly consult with their doctors and discuss medication use and dosages.” 

Testing for Alzheimer’s disease can be a long, costly, and tiresome process for patients, but researchers from Brigham and Women’s Hospital have been working to make the testing process easier on patients.

The group has developed a blood test that would evaluate the level of tau -- the leading protein in the brain associated with Alzheimer’s -- before a patient is even showing signs or symptoms of the disease.

“A blood test for Alzheimer’s disease could be administered easily and repeatedly, with patients going to their primary care office rather than having to go into a hospital,” said Dr. Dominic Walsh. “Ultimately, a blood-based test could replace cerebrospinal fluid testing and/or brain imaging. Our new test has the potential to do just that.”

Though the test is currently in the testing stages, Dr. Walsh is calling it a “transformative breakthrough” based on the early results.

How it works  

Tau is a protein in the brain that is most typically associated with Alzheimer’s. Though tau can develop through a number of different related molecules, the researchers were able to create a model that differentiates between the individual types of tau to ensure that the blood test comes up with the most accurate result.

The researchers have conducted two trials so far with participants from Harvard’s Aging Brain Study and the Institute of Neurology in London. The first group consisted of 65 participants and the second group had 86.

Everyone involved in the study donated samples of plasma and cerebrospinal fluid, which helped the researchers look at the breakdown of the tau protein and see exactly what was linked to Alzheimer’s.

In both tests, the researchers found one strand of tau -- NT1 -- that was effective in predicting and identifying cases of Alzheimer’s.

The next step for the researchers is to open the test up to larger groups of participants to further test its effectiveness on a wider sample. However, these early results proved to Dr. Walsh and his team that they could be on the right track.

“We’ve made our data and the tools needed to perform our test widely available because we want other research groups to put this to the test,” he said. “It’s important for others to validate our findings so that we can be certain this test will work across different populations.”

Fighting Alzheimer’s

While this blood test could potentially change the way doctors go about diagnosing Alzheimer’s, fellow researchers have made strides this year in an effort to better diagnose and treat the disease.

In late September, researchers from the Clinical Memory Research Unit at Lund University in Sweden developed a new brain imaging technique that would help doctors make the most accurate Alzheimer’s diagnoses.

The researchers used a PET scan to evaluate the level of tau in the brain by administering a marker for the protein before the test. The researchers found this new test to be more successful than traditional Alzheimer’s screening methods.

“If the patient has tau in certain parts of the brain, the marker will detect it,” said researcher Oskar Hansson. “The result -- whether Alzheimer tau is present or not -- is very clearly visible on the PET images.”

On the treatment front, researchers found success with a clinical trial for a drug being developed to treat Alzheimer’s.

Amyloid is another protein often found in the brain with Alzheimer’s, and researchers from Biogen and Eisai worked to develop BAN2401 -- an anti-amyloid drug. Though unsuccessful in initial tests, this new and improved version of the drug was found to slow the progression of Alzheimer’s in the study’s clinical trial.

The symptoms and risks associated with Alzheimer’s disease (AD) and dementia have been well-documented, and with over 5.5 million adults across the United States currently suffering, the medical community continues to look for ways to alleviate discomfort and make advancements.

A new study was recently published in the journal American Geriatrics Society that explores the effect exercise has on reducing the risk of falls among Alzheimer’s and dementia patients. The researchers note that over 60 percent of people with AD/dementia fall every year, and they are twice as likely to fall compared with people who don’t have AD/dementia.

More movement

The researchers’ primary goal was to see if AD/dementia patients with neuropsychiatric symptoms -- such as depression, anxiety, irritability, apathy, aggression, hallucinations, etc. -- had a reduced risk of falling when exercise was a regular part of their routines.

The researchers tested this by evaluating the FINALEX trial -- a study that includes a wide demographic of people with AD/dementia and neuropsychiatric symptoms. The study compared participants who had community care -- which didn’t include exercise -- with those who participated in group or home exercise.

The two groups were monitored by physiotherapists for one year and engaged in physical activity for one hour two times per week. The participants were evaluated based on endurance, strength, multitask training, and balance.

One of the biggest takeaways from the study was that the participants who had severe neuropsychiatric symptoms -- such as depression or anxiety -- were at a greater risk for falls, though the exercise proved to be a beneficial method. Additionally, those who had less severe symptoms -- but also didn’t exercise -- still had a high risk of falling.

Those in the exercise groups were found to be at less of a risk for falls, while the opposite was true for those who weren’t in the exercise groups.  

The researchers believe that incorporating exercise into a routine of AD/dementia patients will likely reduce the risk of falls, though more research will need to be done in this area to confirm the results.

Consistent findings

The findings from this study prove to be consistent with a study from earlier this year which found that exercise was linked to improved brain function and can even help prevent memory loss, cognitive function, and diseases like Alzheimer’s and dementia.

Conducted by researchers from UT Southwestern, the study found that keeping active caused nerve fibers in the brain to deteriorate at a much slower rate than for those who didn’t exercise as frequently.

“Evidence suggests that what is bad for your heart is bad for your brain,” said Dr. Rong Zhang of UT Southwestern. “We need studies like this to find out how the two are intertwined and hopefully find the right formula to help prevent Alzheimer’s disease.”

While researchers continue to look for the cause of Alzheimer’s disease, a new study published in Frontiers in Aging Neuroscience explores the connection between the development of the condition and the herpes virus.

Researcher Ruth Itzhaki has spent over two decades studying the relationship between herpes and Alzheimer’s, and in this most recent study she studied the effects that herpes flare ups have on neurons in the brain.

Exploring the connection  

Herpes never goes away entirely, with the condition often flaring up during times of stress or illness. The most severe form of herpes is Herpes Simplex Virus 1 (HSV1), and according to Itzhaki, this strand of the infection could account for “50 percent or more of Alzheimer’s disease cases.”

A key component of Itzhaki’s theory was testing an antiviral drug that could alleviate the risk of senile dementia in people that had herpes.

To get an accurate population sampling to test this theory, Itzhaki utilized data taken from Taiwan’s National Health Insurance Research Database, which documents information on disease and infections.

As nearly all of Taiwan’s population is enrolled in the Database, Itzhaki was able to evaluate three studies published between 2017 and 2018 that described the ways patients with HSV1 were treated by healthcare professionals; the data showed the evolution of those with senile dementia.

Itzhaki found that the antiviral drug was an effective course of treatment for those who were infected with HSV1 and then developed dementia. She also found that those who already have HSV1 areat a much greater risk of later developing senile dementia.

Itzhaki noted that this study focuses on those with the most severe cases of the infection, and future research would have to focus on dementia rates in those with more mild forms of herpes.

Despite this, Itzhaki was confident in the study’s results.

“Considering that over 150 publications strongly support an HSV1 role in Alzheimer’s, these Taiwan findings greatly justify usage of anti-herpes antivirals -- which are safe and well tolerated -- to treat Alzheimer’s disease,” said Itzhaki. “They also incentivize development of an HSV1 vaccine, which would likely be the most effective treatment.”

Recent Alzheimer’s breakthroughs

Alzheimer’s research continues to be a point of emphasis for the medical community, and researchers have made considerable contributions to the field in recent months.

Back in July, a major drug company reported positive results from a clinical trial for a new Alzheimer’s drug. The study involved nearly 900 participants in the early stages of Alzheimer’s, and after 18 months, the drug was found to be successful in slowing the progress of the disease.

Later in the summer, researchers at the University of Adelaide found a link between iron in our cells and a rare genetic mutation that causes Alzheimer’s.

Most recently, researchers from the Clinical Memory Research Unit at Lund University found a new brain imaging technique that would help doctors diagnose Alzheimer’s more accurately. The PET scan involved in the study proved to be more successful than traditional treatments that are currently used to diagnose Alzheimer’s, and the researchers are confident the method will gain popularity worldwide.

Researchers from the Clinical Memory Research Unit at Lund University in Sweden recently published an article detailing a new brain imaging technique that would help doctors diagnose Alzheimer’s more accurately.

In the study, the researchers focused on the spread of two Alzheimer’s-linked proteins throughout the brain -- beta-amyloid and tau. While beta-amyloid can start spreading years before the patient starts showing symptoms of Alzheimer’s, the presence of tau on a brain scan is an indicator that the disease is much further along.

“It is when tau begins to spread that the neurons start dying and the patient experiences the first problems with the disease,” senior researcher Rik Ossenkoppele said in a press release. “If we scan a patient with memory difficulties and he or she proves to have a lot of tau in the brain, we know with a high degree of certainty that it is a case of Alzheimer’s.”

The study shows significant promise for the future of Alzheimer’s research. With the right diagnosis, patients can be put on the right track regarding a medication and diet regimen -- two things that have been linked to improved cognitive function for those living with Alzheimer’s.

The study

The researchers conducted an international study with over 700 participants, and found their method to be successful in correctly diagnosing Alzheimer’s in 90-95 percent of all cases.

“The method works very well,” researcher Oskar Hansson said in the press release. “I believe it will be applied clinically all over the world in only a few years.”

Using a PET scan to determine the level of tau in each patient, the researchers were able to get the most clear and precise image. According to Hansson, the patients received an IV of the tau marker and the PET scan did the rest.

“If the patient has tau in certain parts of the brain, the marker will detect it,” Hansson said. “The result -- whether Alzheimer tau is present or not -- is very clearly visible on the PET images.”

The new test proved to be more successful than traditional treatments that are currently used to diagnose Alzheimer’s. Because of the overlap between Alzheimer’s symptoms and those of other conditions, getting an accurate diagnosis can be difficult. The researchers’ tau test showed its effectiveness -- beating out the often used beta-amyloid-PET scan and MRI scans.

The full study has been published in Journal of the American Medical Association (JAMA).

After a series of disappointments, a major drug company has reported promising clinical trial results from its drug to treat Alzheimer's disease.

Massachusetts-based Biogen and its Japanese partner Eisai jointly announced positive topline results from the Phase II study with BAN2401, an anti-amyloid drug. The buildup of amyloid plaques in the brain is thought to be a key contributor to Alzheimer's.

The study was a large one, involving 856 patients in the early stages of Alzheimer's disease. The study achieved “statistical significance” in its effectiveness at 18 months, slowing the progression of the disease.

Researchers were encouraged because BAN2401 is the same drug that produced disappointing results back in December. The difference, they say, is the drug was only monitored for 12 months. In the second trial, the extra six months produced an improvement.

Mild to moderate side effects

This time, the researchers said BAN2401 showed an acceptable tolerability profile through 18 months of treatment. There were some side effects, but they were characterized as mild to moderate in severity.

All in all, researchers in the field of Alzheimer's disease treatment and study expressed new hope at the results.

“The 18-month results of the BAN2401 trial are impressive and provide important support for the amyloid hypothesis,” said Jeff Cummings, M.D., founding director, Cleveland Clinic Lou Ruvo Center for Brain Health. “I look forward to seeing the full data set shared with the broader Alzheimer’s community as we advance against this devastating disease.”

Alzheimer's is a type of dementia that causes problems with memory, thinking, and behavior. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Eventually, the disease is fatal.

Not a normal part of aging

Aging is a major risk factor, but the Alzheimer's Association points out that the disease is not a normal part of aging. Currently, an estimated 5.5 million people who are 65 or older have been diagnosed with Alzheimer's disease. About 200,000 people under age 65 have what is called younger-onset Alzheimer's.

“The prospect of being able to offer meaningful disease-modifying therapies to individuals suffering from this terrible disease is both exciting and humbling,” said Dr. Alfred Sandrock, executive vice president and chief medical officer at Biogen. “These BAN2401 18-month data offer important insights in the investigation of potential treatment options for patients with Alzheimer’s disease and underscores that neurodegenerative diseases may not be as intractable as they once seemed.”

In an interview with CNBC, Biogen chairman Stelios Papadopoulos called the results an encouraging first step, but he believes further progress is possible. He said a best case estimate for when BAN 2401 could be available to treat patients would be in two to three years.

An existing diabetes drug may hold promise for treating Alzheimer's disease, researchers say.

In experiments on laboratory mice that express the human mutated genes causing Alzheimer's, the drug "significantly reversed memory loss", helping these mice show improved memory formation and learning in maze tests.

The research was conducted at the UK's Lancaster University, where lead researcher Christian Holscher expressed optimism the treatment could heal the neurological damage of chronic cognitive disorders like Alzheimer's disease.

An estimated 5.5 million Americans are living with Alzheimer's disease, which gradually erodes memory function and is ultimately fatal. Despite several promising developments over the last decade, there is still no cure.

More supportive than groundbreaking

James Hendrix, Ph.D., Director of Global Science Initiatives, Alzheimer's Association, says the work is more supportive than groundbreaking, since there are already clinical trials in humans underway.

"We've known for some time that diabetes is a risk factor for Alzheimer's, and other diabetic drugs are currently being tested in clinical trials," Hendrix told ConsumerAffairs.

Hendrix notes that the study required daily injections of the drug, something not as feasible for human patients. And just because the drug appeared to be effective in mice does not mean it would have the same effect on humans.

"It's always unclear how animal data will translate to humans," Hendrix said. "Animal models have been poor in predicting human efficacy for Alzheimer's disease therapies."

Alzheimer's–diabetes link

In recent years researchers have established a link between diabetes and Alzheimer's. According to the Mayo Clinic, a number of studies have suggested that people with diabetes–especially type 2 diabetes–are at higher risk of eventually developing Alzheimer's or other dementias.

One complication of diabetes is damage to blood vessels, which may increase the risk of vascular dementia. Reduced blood flow to the brain, it is believed, may cause reduced memory function.

Despite these and other complicating factors, researchers see reason for hope.

They note the Lancaster study is the first time that a triple receptor drug has been used in multiple ways to protect the brain from degeneration. Its three main ingredients are all growth factors.

That may be significant because problems with growth factor signalling have appeared in the brains of Alzheimer's patients.

Alzheimer's Association scientists say more research is needed. If the drug is shown to have the same effects in people as it does in mice, it would have to go through the Food and Drug Administration (FDA) approval process before it could be cleared as an Alzheimer's disease treatment.

It's an alarming statistic. The Centers for Disease Control and Prevention (CDC) reports deaths from Alzheimer's disease surged 55% from 1999 to 2014.

So, what exactly are we to take from that, given that estimates of future Alzheimer's cases are also rising, since the aging population is growing at a fast pace?

The CDC lists several reasons for the sharp rise in deaths. First, the aging population is growing. The first Baby Boomers turn 70 years-old this year, and each year after another group of Boomers passes the 65 year-old mark, a milestone for the development of Alzheimer's.

People are also living longer, meaning they aren't dying from other diseases. Alzheimer's is a fatal form of dementia, and if someone lives long enough, their chance of developing it -- and dying from it -- increases.

Attributed to other causes

In recent years, doctors have done a better job of diagnosing Alzheimer's. In the past, it is possible people died from Alzheimer's but their deaths were attributed to other causes.

So it doesn't necessarily mean more people are developing the disease than they otherwise would, there are simply more people now who are at risk.

Dr. Anne Schuchat, CDC's acting director, says there's another statistic that should stand out. The number of people with Alzheimer's who died at home jumped from 14% to 25% over the same period. That means caregivers -- primarily a spouse or child -- is bearing a heavy burden.

Burden on caregivers

"As the number of older Americans with Alzheimer's disease rises, more family members are taking on the emotionally and physically challenging role of caregiver than ever before," Schuchat said. "These families need and deserve our support."

Christopher Taylor, Ph.D., lead author of the study, says caregiving becomes even more important in the latter stages of the disease.

"Caregivers and patients can benefit from programs that include education about Alzheimer's disease, how to take care of themselves and their loved one, and case management to lessen the burden of care," he said. "Supportive interventions can lessen the burden for caregivers and improve the quality of care for people with Alzheimer's disease."

Early intervention and diagnosis may also slow development of the disease. People 65 and over should be aware of symptoms such as memory loss, difficulties with problem solving, or misplacing objects. The CDC says an early diagnosis can allow patients and their families to better prepare for medical and caregiving needs at all stages of the disease.

Recently, researchers began developing a potential therapy for concussions, using an FDA-approved drug that helps reduce the harmful effects of swelling. Specifically, they found that the expression of a certain membrane protein called aquaporin-4 increased dramatically after a head injury and caused damage.

While work on that project continues, other experts believe that aquaporin-4 may be a prime target for Alzheimer’s research. A study conducted by researchers from Oregon Health & Science University has revealed a connection between the protein and possible prevention of the brain disease. While it may not materialize into a lasting cure, the researchers believe that their work could contribute to future therapies and prevention strategies.

"It suggests that aquaporin-4 might be a useful target in preventing and treating Alzheimer's disease," said Dr. Jeffrey Iliff, senior author of the study. "However, we aren't under any illusion that if we could just fix this one thing, then we'd be able to cure Alzheimer's Disease."

System breakdown

In a broad sense, Alzheimer’s isn’t a disease that happens all at once – it takes time and is much more progressive. There is currently no cure for it, but several therapies have been developed that may be effective in slowing it down; the researchers believe that aquaporin-4 could provide another.

Aquaporin-4’s functions as part of the brain's glymphatic system. Under certain conditions, it is the protein that allows cerebral-spinal fluid to enter the brain and wash away other proteins like amyloid and tau – the build up of which are main drivers of Alzheimer’s.

The researchers believe that when the system regulating aquaporin-4 breaks down, amyloid and tau are allowed to build up unchecked, leading to nerve damage. They tested this theory by analyzing three groups of 79 donated brains – people younger than 60 with a history of Alzheimer’s, people younger than 60 without a history of any neurological disease, and people over 60 without Alzheimer’s.

They found that aquaporin-4 levels were well organized and ordered in the brains of people without Alzheimer’s or a history of neurological disease, but older brains with Alzheimer’s had very disorganized aquaporin-4 levels. The researchers posit that Alzheimer’s may have developed in these brains due to decreased function to clear away harmful proteins.

Last year, the researchers were given a $1.4 million grant from the Paul G. Allen Family Foundation to continue their research and develop new imaging techniques that could capture brain processes as they happened. The team’s full study has been published in JAMA Neurology. 

There have been many promising breakthroughs in the field of Alzheimer's disease research, giving hope to millions at risk of the devastating disease.

The flip side of that, of course, is when these hopeful promises just don't pan out. So it was with great disappointment that pharmaceutical giant Eli Lilly announced that its promising new drug solanezumab “did not meet the primary endpoint” in it's final, phase 3 testing. The company said it would not seek Food and Drug Administration (FDA) approval of the drug.

Lilly said patients in the trial who were treated with solanezumab did not experience a statistically significant slowing in cognitive decline compared to patients treated with placebo. It dashed the hope raised by previous research.

Solanezumab is a mono-clonal antibody targeting excess amyloid in the brain. It was designed for patients considered to be at risk of Alzheimer's but who had not displayed symptoms of the disease.

Slowing memory loss by 10 years

Researchers were hopeful that doctors might eventually use positron emission tomography (PET scans) to locate beta amyloid as it begins to form plaques in the brains of people with Alzheimer’s disease 10 to 20 years before they show any symptoms of the disease.

The drug would then be administered, removing the harmful protein from the brain before it could begin to build up. Researchers were hopeful it might slow memory loss by at least 10 years.

"The results of the solanezumab EXPEDITION3 trial were not what we had hoped for and we are disappointed for the millions of people waiting for a potential disease-modifying treatment for Alzheimer's disease," said John C. Lechleiter, Ph.D., chairman, president and CEO of Eli Lilly, in a written statement. "We will evaluate the impact of these results on the development plans for solanezumab and our other Alzheimer's pipeline assets."

Lechleiter also issued a statement to the Alzheimer's community in the video below, vowing his company would continue pursuing effective treatments.

Lilly said it would present further findings from the study at the Clinical Trials on Alzheimer's Disease meeting in early December.

Despite potential breaththroughs in Alzheimer's disease research, a cure has remained out of reach.

But researchers at the Cleveland Clinic have presented findings on an experimental drug they say could offer new hope. The drug, called NTRX-07, was used in animal studies and appears to have diminished some of the effects that Alzheimer's has on the brain.

When someone has Alzheimer's disease, his or her brain produces too much of a protein called anyloid plaques. These plaques cause inflammation of the brain that damages neurons. Eventually, the damage is so severe it affects memory and many other functions.

The researchers say NTRX-07 appears to prevent much of this inflammation from occurring, and even preserves the neurons and regenerative brain cells. Lead researcher Dr. Mohamed Naguib, a physician anesthesiologist in the Department of General Anesthesiology at the Cleveland Clinic, says the power of NTRX-07 lies in its specific targeting.

Targets the disease, not the symptoms

“NTRX-07 uses a different mechanism than many other Alzheimer’s drugs currently available, as it targets the cause of the disease, not just the symptoms,” Naguib said.

The researchers made their discovery while testing NTRX-07 as a painkiller, treating other types of inflammation in the body. It worked so well at blunting inflammation that they decided to test it on mice that had been bred to have the kinds of brain issues seen in Alzheimer's patients.

The researchers found that the drug improved the body's ability to remove harmful amyloid plaques and improved memory function. They say it has the added benefit of increasing levels of a protein called SOX2, which they say helps new brain cells develop.

The new drug is expected to enter clinical trials on humans next year, starting with a Phase 1 trial, to check for safety. The Alzheimer's Drug Discovery Foundation has put up $1.7 million to support the developers as they continue to test the drug. The Alzheimer's Association is spending $700,000 to support the Phase 1 trials.

The Alzheimer's Foundation estimates as many as 5.1 million Americans may have Alzheimer's disease. Since age is the main risk factor, there are fears of many more cases as the huge Baby Boom generation enters old age.

New research conducted at Cardiff University could allow for earlier detection of Alzheimer’s disease, a crucial step towards mitigating the damaging effects that it has on people later in life.

Using nearly 300 participants, researchers used blood tests to distinguish certain biomarkers which could predict whether or not someone would develop the disease in the near future.

“Our research proves that it is possible to predict whether or not an individual with mild memory problems is likely to develop Alzheimer’s disease over the next few years,” said Paul Morgan, Director of Cardiff University’s Systems Immunity Research Institute.  

“We hope to build on this in order to develop a simple blood test that can predict the likelihood of developing Alzheimer’s disease in older people with mild, and possibly innocent, memory impairment.”

Influential findings

In order to distinguish the biomarkers, Morgan and his colleagues took blood samples from participants who had mild memory problems and analyzed them for protein content. After a year, the researchers re-assessed each participant.

They found that nearly a quarter of all participants went on to develop Alzheimer’s. Interestingly, those who went on to develop the disease had three proteins in their blood that differed dramatically at the initial screening from those who remained healthy. This evidence could provide some insight into how these immune system proteins contribute to inflammation and Alzheimer’s as a whole.

Morgan believes that these findings could greatly influence how health officials handle Alzheimer’s where he lives in the United Kingdom.

“Alzheimer’s disease affects around 520,000 people in the UK and this number is continually growing as the population ages. As such it is important that we find new ways to diagnose the disease early, giving us a chance to investigate and instigate new treatments before irreversible damage is done,” he said.

The full study has been published in the Journal of Alzheimer’s Disease.

Most of use go on a diet to lose weight or to improve our physical condition. But researchers in Australia have concluded that the Mediterranean diet is not only good for you physically, but mentally as well.

Writing in the journal Frontiers in Nutrition, lead author Roy Hardman from Swinburne University of Technology in Melbourne and his colleagues say the diet appears to slow cognitive decline.

The Mediterranean diet includes a lot of plant foods, like leafy greens, fresh fruit and vegetables, cereals, beans, seeds, nuts, and legumes. There is less dairy and red meat, and olive oil is the preferred source of fat.

"The most surprising result was that the positive effects were found in countries around the whole world,” Hardman said. “So regardless of being located outside of what is considered the Mediterranean region, the positive cognitive effects of a higher adherence to a MedDiet were similar in all evaluated papers."

Heart healthy too

For the most part, doctors recommend the Mediterranean diet for its positive effects on the heart.

“Research has shown that the traditional Mediterranean diet reduces the risk of heart disease,” the Mayo Clinic reports on its website. “The diet has been associated with a lower level of oxidized low-density lipoprotein (LDL) cholesterol — the "bad" cholesterol that's more likely to build up deposits in your arteries.”

And in line with this latest research from Australia, the Mayo Clinic staff notes that the Mediterranean diet has also been associated with a lower incidence of Alzheimer's disease.

The Australian study found the diet improves attention, memory and use of language. In terms of memory, it found notable improves in delayed recognition, working memory, and executive function.

What is it about the Mediterranean diet?

The question is why. What is it about the Mediterranean diet that supports better cognitive function? The authors suggest several things, including a reduction in inflammation, improved vitamin and mineral imbalances, maintaining a healthy weight, and improving polyphenols in the blood.

If you are interested in trying the Mediterranean diet, it is always advisable to discuss any changes in eating patterns with your doctor. Assuming he or she agrees it might be beneficial for you, here are some Mediterranean diet recipes to get you started.

Researchers at Columbia University Medical Center have identified a way they say Alzheimer's disease can spread through the brain.

Their study, published in the journal Nature Neuroscience, says the toxic protein tau jumps from one neuron to another. They say their discovery helps explain why just one area of the brain is affected when Alzheimer's begins, but that much of the brain is damaged in the disease's later stages.

They say it also explains why Alzheimer's always gets progressively worse, never better. Significantly, however, that could change.

“By learning how tau spreads, we may be able to stop it from jumping from neuron to neuron,” said Karen Duff, professor in the department of pathology and cell biology.

Limiting the damage

If doctors were successful in doing so, she says they might be able to stop or limit the progression of the disease.

This isn't the first time researchers have suggested that Alzheimer’s can spread through the brain. The idea first gained traction among medical scientists earlier in the decade when it was found tau moved from neuron to neuron through the brains of mice.

The latest study found that tau travels within the brain, moving from neuron to neuron. That allows it to affect other parts of the brain. Duff says that has important clinical implications.

Important implications

“When tau is released into the extracellular space, it would be much easier to target the protein with therapeutic agents, such as antibodies, than if it had remained in the neuron,” she said.

The new study is just the latest in an area that is receiving intense focus as the large Baby Boom generation enters old age. Health policymakers are concerned about the huge toll on the healthcare system if Alzheimer's cases multiply as predicted.

In one of the most promising recent developments, scientists at the Buck Institute for Research on Aging and UCLA found they could reverse memory loss.

It was an extremely small study, but the researchers say they are excited because it could hold significant potential. The therapy uses existing drugs, along with a strict program of dietary changes, brain stimulation, physical exercise, and sleep optimization.

Alzheimer’s disease strikes older adults, but increasingly, doctors think there are ways to identify young people who will be at risk.

The latest research is published in the online issue of the journal Neurology, and it reveals a genetic risk score that may identify those at risk of the cognitive illness long before any symptoms appear.

Elizabeth C. Mormino, PhD, with Massachusetts General Hospital in Charlestown, Mass., says there is an early stage of the disease that can last a decade or more without the appearance of symptoms.

“Given that current clinical trials are testing whether therapies can slow memory and thinking decline among people at risk for the disease, it is critical to understand the influence of risk factors before symptoms are present,” Mormino said.

The study

The study looked at people with dementia and those without it, assigning each a numeric score based on the presence of high risk genes. The participants were examined for common Alzheimer’s markers, including a decline in memory and thinking skills, clinical progression of the disease, and the volume of the hippocampus, which is the memory center of the brain.

The research team next looked at any links between the risk score and hippocampus size in 1,322 healthy, younger participants between the ages of 18 and 35.

Results

Even among older people who had no dementia – but who had a higher genetic risk – there was a stronger likelihood of worse memory and smaller hippocampus at the start of the study.

Over the three years of the study, a higher genetic risk score was also associated with greater longitudinal memory and executive function decline and clinical progression of the disease.

The risk score was also linked to overall disease progression, with 15 of 194 participants who were cognitively normal at the start of the study developing mild cognitive impairment or Alzheimer’s disease. Of the 332 subjects with mild cognitive impairment at the start of the study, 143 developed Alzheimer’s disease after three years.

Mormino concedes it was a small study, but she says further research could help doctors better identify people at high risk of dementia at a much earlier age and begin preventive treatments sooner.

Researchers are still working hard when it comes to understanding how Alzheimer’s disease works, and that commitment may be beginning to pay off. A study conducted at the Douglas Mental Health University Institute may have uncovered the driving force behind the disease’s signature symptom – the development of dementia.

For a while now, scientists have suspected that dementia developed in Alzheimer’s patients because of the presence of two proteins, called amyloid and tau, respectively. However, they were uncertain about which protein, if either, was the driving force behind the dementia symptom. It turns out that it may be both.

A study has found that both amyloid and tau work in tandem to create toxic effects that lead to brain damage. It is the first piece of definitive evidence that connects the two proteins to cognitive damage sustained by otherwise cognitively intact individuals.

Challenging previous theories

While the build-up of amyloid and tau proteins can be dangerous on their own, the researchers found that their ability to cause harm was increased when they were together.

“We specifically found that both proteins mutually enhance their individual toxic effects and cause a brain dysfunction considered to be a signature of [Alzheimer’s disease]. This finding challenges previous polarized theories that a single protein abnormality was the major driving force of disease progression,” said Dr. Pedro Rosa-Neto, lead scientist of the study.

The researchers came to their conclusions after analyzing 120 cognitively intact individuals over a two-year period. Participants had their amyloid and tau levels monitored for the duration of the study. Based on the changing levels that the researchers observed, they were able to see how the proteins reacted with each other and then predicted which participants were the most likely to suffer brain damage as a result of Alzheimer’s disease.

New therapies

The researchers believe that their discovery may help in the development of new, more effective therapeutic approaches that target both proteins in the brain.

“Until now, therapeutic clinical trials have targeted a single pathological process. Our result paves the way for new therapeutic strategies for prevention or stabilization of [Alzheimer’s disease]. For example, combination therapies should be used simultaneously against both amyloid and tau protein accumulation,” said Dr. Tharick A. Pascoal, lead author of the study.

The full study has been published in the journal Molecular Psychiatry.

Eligible bachelors may want to consider adding “highly intelligent” to the list of qualities Mrs. Right should possess. If you’ve already partnered up with one? Good news: she may prevent you from getting dementia later in life.

Marrying an intelligent woman can act as a “buffer” against the disease, according to Lawrence Whalley, emeritus professor of mental health at the University of Aberdeen. During an Oxford University Literary talk called “Dementia: How Can We Protect Ourselves,” Whalley explained that brainy ladies have an effect on their partner’s brain similar to writing, reading, or visiting a museum.

Previous research has found a link between these types of intellectual challenges and a lowered risk of Alzheimer’s (the most common form of dementia). But spending your life with an intelligent woman could be like spending your life with a living, breathing crossword puzzle.

“The thing a boy is never told he needs to do if he wants to live a longer life -- but what he should do -- is marry an intelligent woman,” Whalley told the Daily Mail. “There is no better buffer than intelligence.”

Slows the aging process

It's estimated that 47.5 million people worldwide currently live with dementia, and that number is expected to nearly double every 20 years. Certain childhood experiences can put people at risk for dementia, but later experiences can help reduce that risk.

“Studies have shown that the death of a mother before the age of five is a very important risk factor for dementia in later life,” said Whalley. However, choosing an intelligent partner who provides interesting, mentally stimulating conversations could help prevent Alzheimer's.

A study revealed to scientists that environmental factors can also have a big impact on a person’s mental health. In a side-by-side comparison of two brain scans, Whalley noted that people who showed physical signs of the illness but had no symptoms were “highly intelligent” and in “high-powered jobs.”

The threat of Alzheimer’s disease continues to weigh heavily on nations across the world. An increasing number of people will soon reach the age where the disease may start to affect them, and experts believe that unless new treatment options are discovered, over 100 million people across the globe will be affected by it by the year 2050.

With the timeline constantly shrinking, medical experts and scientists are doing their best to find ways to avert the cognitive decline that is the trademark of the disease. One such researcher is Dr. Riqiang Yan, who recently discovered a way to disrupt the formation of dystrophic neurites (DN), constructions that are especially prominent in the brains of Alzheimer’s patients.

Improving cognitive function

DNs are made up of nerve components that have a tendency to cluster together in the brain, especially in people over the age of 65. Dr. Yan and his team were able to trace these formations back to a problem in the endoplasmic reticulum (ER), which is a structure found in our cells. When DNs contain too many proteins, they can warp the structure of the ER and impair cellular function.

The researchers found that this excess of proteins was especially prominent in Alzheimer’s patients. One protein in particular, called RTN3, was not easily found in the brains of patients under the age of 60, but flourished in those over the age of 65.

When the researchers decreased concentrations of RTN3 in a rodent model, they found that the formation of DNs was also stunted. This could mean that targeting this particular protein could lead to improved cognitive function in Alzheimer’s patients and the elderly, although much more testing will need to be conducted before the theory could be tested on humans.

The full study has been published in the journal Molecular Psychiatry. 

Doctors aren't sure what causes Alzheimer's disease, a cognitive degeneration that is ultimately fatal. There may be a number of contributing factors. That may be why it has been so difficult to find a cure.

However, intriguing research is exploring the link between a Western diet and sedentary lifestyle and the risk of developing the disease.

Tufts University researchers experimented with mice and found that prolonged consumption of the Western diet led to a dramatic increase in immune response activity in the brains of all mice, including those that don’t model Alzheimer’s disease.

The diet greatly increased the activity of microglia, which function as the brain’s immune cells. It also stimulates monocytes, circulating white blood cells that may cross into the brain in response to immune signaling.

The researchers were following up on previous findings that suggest some elements of the western diet have been associated with the development of peripheral inflammation over time.

Immune activity link

The researchers conclude that it is becoming more likely that immune activity in the brain increases Alzheimer’s disease risk.

The Alzheimer's Association has long stressed diet as one way to help reduce the risk of developing the disease.

It recommends eating a heart-healthy diet, saying it will benefit not just your body, but your brain.

“In general, this is a diet that is lower in fat and higher in vegetables and fruit,” the group says on its website. “Research in the area of the relationship between diet and cognitive functioning is somewhat limited, but it does point to the benefits of two diets in particular: the DASH (Dietary Approaches to Stop Hypertension) diet and the Mediterranean diet. These diets can help reduce heart disease and may also be able to reduce risk of dementia.”

Physical activity

The association has also been an advocate for physical activity, calling it a valuable part of any overall body wellness plan that is associated with a lower risk of cognitive decline.

Regular exercise will increase the blood flow to your brain and body, providing additional nourishment while reducing potential dementia risk factors such as high blood pressure, diabetes, and high cholesterol.

It's also important to start these habits at a young age, but always clear any new exercise program with your doctor.

Researchers from around the world have been working tirelessly towards understanding, and hopefully one day curing, Alzheimer’s disease. While experts still do not understand every facet of the cognitive ailment, a team from Lund University in Sweden may have taken a crucial step towards that goal.

The researchers have found that amyloid plaque, the build-up of which is a marker for Alzheimer’s, is much more versatile than previously suspected. Before now, many believed that the build-up of amyloid plaque was hereditary; in short, if you possessed the gene that caused your body to overproduce amyloid plaque, then you were more likely to develop Alzheimer’s.

However, researchers have found that having this hereditary trait is not necessary for developing the disease. In fact, one does not need any such gene in order to develop Alzheimer’s.

“In our study, we show that accumulation of amyloid in the brain is associated with high levels of specific amyloid peptides in the cerebrospinal fluid,” said Niklas Mattsson, a researcher at Lund University. “This means that overproduction of amyloid beta may contribute to development of Alzheimer’s disease in some people, even if they do not carry the hereditary risk gene for Alzheimer’s.”

Increasing understanding

The researchers made their discovery after examining patients without the hereditary gene for amyloid plaque build-up. Over 330 people participated in the study – they included people with mild cognitive disorders (which can be an indicator for Alzheimer’s) and a control group who had no impairment.

Cerebrospinal fluid samples were collected from each participant and then examined. Results showed that there were increased levels of amyloid beta in some patients in the experimental group, even though they did not have the hereditary gene.

“We were surprised by the results. Our study emphasizes that Alzheimer’s is probably a more heterogeneous disease than we previously believed,” said Mattsson. “The results are important because they increase the understanding of how Alzheimer’s disease arises,” added Oskar Hansson, a reader at Lund University and consultant at Skåne University Hospital.

Possible medical benefits

While future studies will be necessary in order to verify the results, the researchers are hopeful that their work will help in the development of new medications.

“Our hope is that this and other similar studies can increase the possibilities of personalizing treatments that slow down the disease in the future,” said Hansson.

The results of the study have been published in the journal Nature Communications. 

People are living longer, reaching age 90 and beyond in greater numbers than ever before.

But as you age, keeping engaged in social activities and using a computer to email friends and stay connected to the world may be key to an improved quality of life.

A study to be presented at a medical conference next month finds an active brain appears to help older adults reduce their risk of developing memory and thinking problems.

“The results show the importance of keeping the mind active as we age,” study author Janina Krell-Roesch, with the Mayo Clinic in Scottsdale, Ariz., said in a statement. “While this study only shows association, not cause and effect, as people age, they may want to consider participating in activities like these because they may keep a mind healthier, longer.”

The study followed nearly 2,000 people who were at least 70 years old and had no cognitive impairment. Four years later they were tested again and those who had begun to experience memory decline were identified.

42% less likely to suffer memory problems

Each participant's profile went into detail about their mental activities, including their computer use.

The study found that people who used a computer once per week or more were 42% less likely to develop memory and thinking problems than those who did not.

Engaging in regular social activity was also helpful, but not quite as effective as regular computer use. Those engaging in social activities were only 23% less likely to develop cognitive issues than people who didn't.

Other activities that were somewhat effective in keeping aging minds sharp included crafts, such as knitting; reading regularly; and playing games.

It turns out there is a difference between the symptoms of Alzheimer's disease and the disease itself.

Good health and physical and mental exercise as you age may in fact delay the onset of Alzheimer's symptoms, but researchers writing in a medical journal of the American Academy of Neurology say it won't prevent the disease.

The study centered around people who carry a gene linked to Alzheimer's, the so-called APOE4 gene. An estimated 20% of the U.S. population carries it.

The researchers divided people with the gene into two groups. One group stayed mentally active in middle age and one didn't.

The mentally active group had lower levels of proteins, called amyloid plaques, that can build up in brain tissue and lead to Alzheimer’s disease than those who did not stay mentally active.

The difference was significant. The mentally active group had the same plaque build-up at age 79 that the non-active group had at 74.

“Recent studies have shown conflicting results about the value of physical and mental activity related to the risk of developing Alzheimer’s disease, and we noticed that levels of education differed in those studies,” study author Prashanthi Vemuri of the Mayo Clinic, said in a release. “When we looked specifically at the level of lifetime learning, we found that carriers of the APOE4 gene who had higher education and continued to learn through middle age had fewer amyloid deposition on imaging when compared to those who did not continue with intellectual activity in middle age.”

Misdiagnosis

Some patients are diagnosed with Alzheimer's when they are actually suffering from frontotemporal dementia, which delays the correct treatment for them.

“Some people cannot tell frontotemporal dementia from Alzheimer’s disease,” Dr. Joseph Masdeu, director of the Nantz National Alzheimer Center at Houston Methodist Hospital, said in a release. “However, these diseases have different symptoms and treatments. And with advances in neuroimaging, we can see a clear difference in how frontotemporal dementia manifests in the brain.”

The accumulation of the protein beta amyloid in Alzheimer's can lead to excess production of an abnormal form of the important brain protein, tau.

But beta amyloid is absent in frontotemporal dementia, and a different abnormal form of tau is detected.

“A misdiagnosis of Alzheimer’s can prevent a person with frontotemporal dementia from participating in future trials for this group of disorders” Masdeu said.

Since potential Alzheimer’s treatments would not help a patient with frontotemporal dementia, misdiagnosed patients participating in Alzheimer’s clinical trials can skew that data and prevent the advancement of those treatments, Masdeu said.

If you are an aging Baby Boomer, should you be eating more fish?

There have been studies suggesting that fish oils are good for brain function and may delay or prevent dementia. At the same time, fish can contain mercury, picked up from the environment, and mercury is believed to contribute to cognitive impairment.

Researchers at Rush University Medical Center have studied the relationship between mercury and diseases associated with dementia. They report that as mercury levels rise with seafood consumption, there were no associations with harm to the brain.

Instead, they discovered that seafood consumption was associated with less Alzheimer's disease neuropathology, in spite of the increased mercury levels.

Helps people most at risk

However, the the protection associated with seafood was only seen in people with a common genotype (APOE-?4) that increases the risk of developing Alzheimer's disease. In other words, for people at risk of developing Alzheimer's disease, eating seafood made it less likely.

"Seafood consumption is promoted for its many health benefits even though it's contaminated by mercury," study leader Martha Clare Morris, said in a release. "Since mercury is a known neurotoxin, we wanted to determine whether seafood consumption is correlated with increased brain mercury levels in older adults, and also whether seafood consumption or brain mercury levels are correlated with brain neuropathologies."

The researchers conclude that seafood consumption was significantly correlated with less Alzheimer disease pathology. In particular, it was associated with lower density of amyloid plaques in the brain and less severe and widespread tangles within the neurons. Plaques and tangles are normally present in Alzheimer's patients.

Mercury's role in dementia

A 2010 German study, published on a National Institutes of Health (NIH) website, concluded that exposure to inorganic mercury led to “significant memory deficits.” Some autopsy studies found increased mercury levels in brain tissues of AD patients.

The issue, then, may be the extent of mercury levels found in seafood. The Rush University researchers say it's likely that the types of fish consumed by the study participants reflect the top 10 consumed species in the U.S., which have low to moderate levels of mercury.

How much seafood should you eat? A report by the Harvard School of Public Health notes that it is a controversial subject. The report suggests striking a healthy balance, with fish showing up on the menu once or twice a week.

If you want to know what kind of fish is best, EatingWell.com has compiled a list of the best and the worst.

Researchers aren't completely sure what causes Alzheimer's disease. That said, an intriguing theory has emerged and gained a little more traction after a series of autopsies. Information about it has been published in Swiss Medical Weekly.

The autopsies were performed on a small number of people who had died from a brain disease known as Creutzfeldt-Jakob disease (CJD). They all had one thing in common.

Long before their deaths, the victims had all undergone a rare procedure in which the membrane covering the brain and spinal cord is taken from a cadaver and grafted onto a healthy brain. It turns out the grafted material was contaminated with the prion protein associated with CJD.

Signs associated with Alzheimer's

During these autopsies, the researchers noticed something. Five of the brains being examined also had some of the signs that are associated with Alzheimer's disease.

What does it mean? The researchers conclude that the presence of the protein in young people is “highly unusual” and suggests a causal relationship to the grafts from the cadavers. The researchers further said it is possible the transplanted material was contaminated with small traces of the protein which possibly could have also been a trigger for Alzheimer's.

Though far from conclusive, the results fit with a few researchers' theory that, in a few cases, Alzheimer's disease might be transmissible.

September study

Back in September, the journal Nature published a study suggesting the abnormality that triggers Alzheimer's could, at times, be transmitted to a healthy person by transplanting tissue containing the abnormality. But even the study authors were careful to point out they were not suggesting Alzheimer's is contagious.

However, the Swiss findings may cause further study in this area. Currently, the research into Alzheimer's is focusing on earlier diagnosis and a possible cure.

According to the National Institute on Aging, current research ranges from the basic mechanisms of Alzheimer's to managing the symptoms and helping families cope with the effects of the disease.

As we reported in September, Johns Hopkins has received a major grant to run clinical trials on an epilepsy drug that researchers believe will show promise as a way to prevent Alzheimer's.

What's a “senior moment” and what's a sign of more serious memory issues? That's a question seniors and their families often ask, and until now there have been few clear-cut answers.

But researchers at the University of California, San Diego School of Medicine and Washington University in St. Louis have launched a major clinical trial to find out if mental decline in seniors can be slowed or halted through exercise and other health-related interventions.

Specifically, the trial will focus on using Mindfulness Based Stress Reduction (MBSR), physical exercise, and health education. Researchers will be trying to find whether they can influence cognitive processes, such as attention and memory, in older adults.

“Our overall goal is to find out how to improve memory and concentration in older people,” said Julie Wetherell, PhD, co-principal investigator and professor in UC San Diego School of Medicine’s Department of Psychiatry.

Timely trial

The trial starts at a time when about 10,000 Baby Boomers are turning 65 every day. In the next few decades the country’s senior population will almost double, from 43 million in 2012 to nearly 84 million by 2050.

“As our society ages, we want to preserve cognitive function and enhance it if possible,” said Wetherell. “We know the brain is capable of growing new connections into old age. If we demonstrate that one, two or all three of these interventions work, it will be good news for older people who want to maintain and improve their cognitive abilities.”

Holiday health assessment

Holiday gatherings are a good time for family members to observe the cognitive function in parents, grandparents, aunts, and uncles. The holidays can be especially useful if several months have passed since older and younger family members have been together.

"If you haven’t seen your elderly loved one in a while, you might be more likely to notice changes in their memory and behavior that worry you," said Dr. Gregory Jicha, of the University of Kentucky Sanders-Brown Center on Aging.

Jicha says these are some troubling signs to watch for:

• It's normal for someone to forget a date or a name but suddenly remember it later. What isn't normal is if they ask for the same information repeatedly, or struggle to recall important dates.
• Are they having trouble following a recipe? Problem-solving skills can deteriorate in someone with Alzheimer's disease (AD).
• Do they get lost when driving to a familiar location? If they have difficulty completing familiar tasks, it might be a sign of AD.
• Healthy people occasionally struggle to find the right word, but using the wrong word -- particularly if they call something by the wrong name – could be something to worry about.
• Poor judgment: are they giving lots of money to telemarketers or charities?
• Poor hygiene.
• Personality changes: are they suddenly irrational, fearful, or suspicious?

Jicha says any of these observations should be discretely shared with other family members and a doctor.

Early detection is important in cognitive diseases like Alzheimer’s, and researchers are hard at work trying to find ways to diagnose these illnesses earlier.

A neuroscientist at Florida Atlantic University says he has developed a simple, three-minute test to identify the onset of Lew Body disease (LBD), a little-understood condition but the second-most-common cognitive disease after Alzheimer’s.

LBD affects more than 1.3 million Americans, but it is poorly recognized, meaning diagnosis is often significantly delayed. Patients with LBD simultaneously experience losses in cognitive function, mobility, and behavior.

Actor Robin Williams had this form of dementia. So did NHL coach Alger Joseph “Radar” Arbour.

Misdiagnoses common

“Most patients never receive an evaluation by a neurologist skilled in the diagnosis of Lewy body dementia, and significant delays and misdiagnoses occur in most patients with this disease,” said Dr. James E. Galvin, who developed what he calls the Lewy Body Composite Risk Score (LBCRS).

The LBCRS is a brief rating scale that is completed by a clinician to measure the symptoms highly associated with the LBD. With the tool, which takes about three-minutes to administer, a clinician can determine the type of dementia affecting the patient.

Results of a study deploying the LBCRS appear promising. In a real-world clinical setting, the LBCRS was able to discriminate between Alzheimer’s disease and LBD with 96.8 percent accuracy.

“Early detection of Lewy body dementias will be important to enable future interventions at the earliest stages when they are likely to be most effective,” said Galvin. “Our study provides evidence-based methodology that will have applications in clinical practice, participation in clinical trials, prevention studies, community surveys, and biomarkers research.”

A new discovery in Alzheimer’s research could prove to be integral in slowing the cognitive decline that makes the disease so difficult to manage. Researchers from the Vlaams Instituut voor Biotechnologie (VIB) and Katholieke Universiteit Leuven (KU Leuven) in Belgium have discovered that a certain protein called GPR3 may hold the key to reducing amyloid plaque build-up in the brain.

Researchers believe that the accumulation of proteins in the brain –specifically amyloid plaques – play a major role in the development of Alzheimer’s disease. Over time, proteins in the brain are segmented into different parts – one type of segment is called an amyloid-β peptide.

When amyloid-β peptides build up, they become amyloid plaques, which can block the pathways between nerves and the brain. Eventually, this forces many of the brain’s networks to shut down, which compromises healthy mental function. This causes dementia to develop, which is a hallmark of Alzheimer’s disease.

Researchers at VIB and KU Leuven were able to discover and test proteins in order to determine which ones played a major role in amyloid plaque build-up. “We discovered that G protein-coupled receptor 3 (GPR3), a protein expressed in the brain, plays a significant role in the generation of amyloid-? peptides and accumulation of amyloid plaques,” said Amantha Thathiah, leader of the research team.

“Our research indicates that the absence of GPR3 alleviates the cognitive decline and reduces amyloid pathology in multiple disease-relevant models. These studies identify GPR3 as a therapeutic target for [Alzheimer’s disease] and provide a significant level of validation necessary for the future of [Alzheimer’s disease] drug discovery."

Thathiah and her team were able to test their theory by using mouse models. By lowering GPR3 levels in the brain, researchers found that they were able to improve cognition in test subjects. Further examination of post-mortem brain tissue showed that GPR3 levels were high, suggesting that the protein progressed the disease in those subjects.

By testing multiple models, the researchers hope that their work will help form new therapies to combat Alzheimer’s disease. “Given the vast resources required to develop and evaluate a new therapy, demonstrating the relevance of research findings in multiple disease-relevant models is crucial. Our research provides exactly this level of validation,” said researcher Bart de Strooper.

The full study has been published in the journal Science Translational Medicine. 

A clinical trial is underway to determine whether a new drug that attacks beta amyloid in the brain could delay the onset of Alzheimer's disease.

If it can, scientists say it would be a breakthrough in the treatment of this disease that robs victims of their memory and ultimately causes death.

Beta amyloid is a protein that can form in the brain and previous research has suggested that when it builds up it plays a major role in the development of Alzheimer's.

The drug is a mono-clonal antibody called solanezumab, which targets excess amyloid in the brain. It is being given to subjects ages 65 to 85 who are deemed at risk for Alzheimer’s disease-related memory loss but who have not yet shown signs of the disease.

Treatment before symptoms appear

If successful, doctors might eventually use positron emission tomography (PET scans) to locate beta amyloid as it begins to form plaques in the brains of people with Alzheimer’s disease 10 to 20 years before they show any symptoms of the disease.

The idea is to remove that harmful protein from the brain before it can begin to build up. Researchers think it could delay memory loss by at least 10 years.

The trial is being carried out at the Nantz National Alzheimer Center at Houston Methodist Hospital.

The center was established with major financial support from NBC sportscaster Jim Nance and his wife Courtney, who have campaigned to increase funding for research and generate awareness of dementia and Alzheimer’s disease, as well as the possible effects that concussions and traumatic brain injuries have on these diseases.

“It is encouraging to be able to detect excess beta amyloid with PET technology in people predisposed to Alzheimer’s and then try to lower the amyloid levels with solanezumab,” said Dr. Joseph Masdeu, principal investigator of the study.

However, Masdeu says there appears to be a point in the development of Alzheimer’s where removing beta amyloid does not reverse or stop the disease progression because too much damage has been done. That's why it is crucial to identify patients early, before they begin to display symptoms.

Approximately 1,000 adults are expected to participate in more than 60 sites, besides the Nance Center, across the United States, Canada, and Australia.

IVIG shows promise

Meanwhile, in another trial, the blood product intravenous immunoglobulin, or IVIG, was found to reduce brain atrophy and cognitive decline in patients in the early, pre-dementia phase of Alzheimer’s disease.

IVIG is extracted from the plasma of more than 1,000 blood donors and contains antibodies to amyloid. Researchers at the Sutter Institute of Medical Research designed the study to see if a course of IVIG could be a practical way to reduce the effects of Alzheimer's when administered before a patient develops dementia.

Researchers say the study showed promising results during the first year after treatment in the form of reduced brain atrophy as well as reduced development of dementia.

“This research shows some evidence that IVIG could prevent brain atrophy and delay the onset of Alzheimer’s disease in patients who are in the beginning stages,” said Shawn Kile, M.D., Sutter Neuroscience Institute neurologist and principal investigator of the IVIG study. “My hope is that our study will lead to additional investigations of this treatment strategy so we can eventually conquer this devastating disease.”

A lot of high-powered research is currently aimed at Alzheimer's disease, as the huge Baby Boom generation moves into old age.

Since age is a principal risk factor, health officials are concerned that the memory-robbing and ultimately fatal disease could become an epidemic. Scientists working independently have recently uncovered new information that may lead to improved treatments. Both involve genes.

At Indiana University (IU), a research team has identified an immune system gene associated with higher rates of amyloid plaque buildup in the brains of Alzheimer’s patients and older adults. This plaque is believed to be a primary cause of the disease.

Potentially more harmful gene

The variant occurs in the IL1RAP gene, and researchers say it is associated with even more plaque build-up than the previously discovered APOEe4 allele gene.

The new study found that the amyloid-associated IL1RAP variant was also associated with a faster loss of memory and overall cognitive ability.

"These findings suggest that targeting the IL1RAP immune pathway may be a viable approach for promoting the clearance of amyloid deposits and fighting an important cause of progression in Alzheimer's disease," said Andrew Saykin, director of the Indiana Alzheimer Disease Center and the national Alzheimer's Disease Neuroimaging Initiative Genetics Core.

In unrelated research, scientists at State University of New York (SUNY) have found that women who have the APOEe4 allele gene variant experience a steeper decline in body mass index (BMI) after age 70 than those women without the version of the gene, whether they go on to develop dementia or not.

Weight may be a clue

Why is this important? Because it adds to a body of evidence suggesting that body weight change may provide a tell, aiding doctors in the diagnosis and management of Alzheimer's disease.

Research team leader Deborah Gustafson says women tend to follow a U-shaped relationship between age and BMI, a common marker of overweight and obesity. From the time they enter middle age to the time they reach 70 years of age, the average adult tends to gain weight. In other words, that's the norm.

After age 70, weight tends to decrease on average. This weight change over the life course may be due to aging, changes in body composition, energy metabolism, sensory changes, and changes in the brain related to regulation of basic body processes.

But the researchers found that among adults who develop dementia, this pattern is altered. Studies have shown that being more overweight or obese in mid-life may increase risk for dementia. Studies have also shown that after age 70 years, adults who develop dementia may lose weight more rapidly compared to those who do not develop dementia.

Protective pounds

Being a little overweight in later life is protective against both dementia and death.

Gustafson says those with the APOEe4 allele gene experience greater or steeper decline in BMI after age 70 years, even if they don't develop dementia. The discovery, she says, may aid in understanding of how doctors can better intervene among those at highest risk for dementia.

Alzheimer's disease affects more than 5 million older Americans and there is currently no therapy proven to halt or reverse the underlying cause of the progressive symptoms of dementia, though recent research has seemed promising.

Researchers are increasingly focused on mechanisms involved with the deposit and clearance of amyloid plaques, particularly in early stages when symptoms are mild or not yet present.

Since age is the major risk factor for Alzheimer's disease, health officials worry that the huge and aging Baby Boom population is going to lead to a staggering increase in the affliction.

Now comes word that British health researchers have concluded that longer life spans mean more people will suffer dementia at some point. Their report, produced for Alzheimer's Research UK, predicts that one in three Britons born this year will be affected by loss of cognitive ability at some point in their lives.

Alzheimer's is the most common brain disease but is not the only one. The various dementias result in the loss of brain cells and impair the brain’s ability to function properly.

Early symptoms can include problems with memory and thinking. As more brain cells die, physical functions such as walking and even swallowing can be affected. There is no cure, although a new drug that may slow or stop Alzheimer’s will soon undergo Phase 3 clinical trials.

While the research focuses on people living in the UK, similar results can be expected for other Western countries, including the U.S.

More women than men

The report estimates that 32% of people born in the UK in 2015 will develop dementia during their lifetime. Women are more likely than men to develop the disease – 37% to 27%.

“These figures underline a stark reality: as people are living longer, more and more people will develop dementia in the future if action is not taken now to tackle the condition,” said Matthew Norton, Head of Policy at Alzheimer’s Research UK. “It’s wonderful news that each generation is living longer than the last, but it’s important to ensure that people can enjoy these extra years in good health.”

The research team previously concluded that if science is able to produce a treatment that could delay the onset of dementia by five years, it would reduce the number of cases by one-third. Major research is underway to do just that.

Research

A year ago researchers in California reported stunning results after a small study of patients just diagnosed with Alzheimer's disease. They administered a novel and complex treatment they say restored memory function in nine out of ten study participants.

The treatment consists of a 36-point therapeutic program involving comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific drugs and vitamins, and multiple additional steps that affect brain chemistry.

It is the first Alzheimer's research to suggest that memory loss in patients may be reversed, and that improvement can be lasting.

For the first time, a drug designed to prevent or delay the onset of Alzheimer's disease will be tested in a major clinical trial, the first step in bringing the drug to market.

Researchers at Johns Hopkins University say they are getting $7.5 million from the National Institutes of Health (NIH) for a Phase 3 trial of the drug levetiracetam, scheduled to start early next year.

Levetiracetam is not a new drug. It has been commonly prescribed for more than a decade to treat epilepsy. Johns Hopkins neuroscientist Michela Gallagher and colleagues have shown that a form of the drug calms hyperactivity in the brain of patients with a condition known as amnestic mild cognitive impairment (aMCI), in which memory impairment is greater than expected for a person’s age.

Doctors believe it also greatly increases risk for Alzheimer’s dementia. More than 5.6 million Americans and 25 million people globally suffer from aMCI.

Gallagher says scientists believe overactivity in aMCI is a strong predictor of who will ultimately get Alzheimer's, a progressive brain disease that is ultimately fatal.

“We expect our upcoming trial to demonstrate efficacy in preserving cognition and memory in aMCI patients while delaying progression to the clinical stage of Alzheimer’s dementia,” Gallagher said.

Skipping first two phases

Because levetiracetam is already an approved drug for epilepsy, it will skip the first two phases of trials. In a Phase 1 trial, a drug is tested on a small group of people for safety. In a Phase 2 trial, it is tested on a small group to determine if it is effective and has harmful side effects.

In a Phase 3 trial, a drug or treatment is given to large groups of people to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely.

If a drug passes a Phase 3 clinical trial, the FDA usually allows it to be marketed for the purpose for which it was tested.

Public-private partnership

The trial will be carried out in a public-private partnership between the NIH’s National Institute on Aging, Johns Hopkins, and the biopharmaceutical company AgeneBio. Patients will receive a mild dose of levetiracetam, called AGB101, in an extended release once-a-day tablet at approximately one-fifth to one-twelfth of the dose most commonly prescribed for epilepsy. Other patients will receive a placebo. The trial is expected to last 18 months to two years.

Other promising Alzheimer's treatments have yet to come to the clinical trial stage but appear to be in the pipeline. As we reported late last year, researchers at UCLA believe they are on the cusp of a breakthrough in which memory loss can not only be slowed but lost memories restored in patients in the early stages of Alzheimer's disease.

There has been an increased urgency associated with Alzheimer's research since the large Baby Boom population began entering the period of highest risk. While Alzheimer's is not a normal part of aging, the Alzheimer's Association says people age 65 and older are at the highest risk.  

A team of international researchers set out to study how genes reveal a person's biological age and how it might differ from his or her chronological age.

They ended up developing a blood test that just might reveal the risk of cognitive decline, including the development of Alzheimer's disease.

The seven-year collaborative study at King’s College London, Karolinska Institutet in Sweden and Duke University, used a process called RNA-profiling to measure and compare gene expression in thousands of human tissue samples.

The researchers found that the activation of 150 genes in the blood, brain and muscle tissue signaled good health when someone reached age 65. They were then able to develop a healthy aging formula that can be used to show how well a person is aging.

Range of aging scores

The formula contains a extensive range of scores of people born the same year, but with very distinct aging characteristics. A high score correlated to a lower chronological age while a low score suggested a person is aging faster than someone their age should.

Perhaps more important, people with low scores were more likely to suffer from cognitive decline. The takeaway, say researchers, is it should be possible for a molecular test to translate into a simple blood test to predict those most at risk of Alzheimer’s disease or other dementia.

Whether someone scored high or low on the aging chart seemed to have little to do with lifestyle factors. For example, if someone were overweight of suffered from heart disease seemed to have little bearing on how fast aging was occurring.

First practical aging test

The researchers say the real significance of their findings may be the possibility of the first practical and accurate test for the rate at which individual bodies are aging. If this is the case, they say it could lead to new insights in research because age is a critical factor in almost every area of medicine.

The work follows previous research that has shown not everyone ages at the same rate.

“Given the biological complexity of the aging process, until now there has been no reliable way to measure how well a person is aging compared with their peers,” said James Timmons, of King’s College London and lead author of the study. “Physical capacity such as strength or onset of disease is often used to assess ‘healthy aging’ in the elderly but in contrast, we can now measure aging before symptoms of decline or illness occur.”

Doctors have long known that some people seem to show the signs of aging earlier than others of the same chronological age, but haven't known exactly why.

Reducing age-related disease

“We now need to find out more about why these vast differences in aging occur, with the hope that the test could be used to reduce the risk of developing diseases associated with age,” Timmons said.

Timmons and his colleagues say their findings, published in the journal Genome Biology, could help improve management of age-related disease by identifying people most at risk of diseases affected by age, as well as improve the way anti-aging treatments are evaluated.

Alzheimer's researchers at the University of Montreal Hospital have made an odd discovery. They believe it could unlock the secret to the age-related disease.

When the researchers examined brains of patients who died from Alzheimer's, they discovered the brains all contained droplets of fat. Could there be a connection?

"Our experiments suggest that these abnormal fat deposits could be a trigger for the disease", said Karl Fernandes, a researcher at the hospital and a professor at the University of Montreal.

Astonishing discovery

The study started out as a way to solve the mystery of why the brain's stem cells don't repair brain damage in people with Alzheimer's like they would with other brain injuries and diseases. Doctoral student Laura Hamilton, who was conducting the research, said she was astonished to find fat droplets near the stem cells on the inner surface of the brain in mice predisposed to develop the disease.

"We realized that Dr. Alois Alzheimer himself had noted the presence of lipid accumulations in patients' brains after their death when he first described the disease in 1906,” she said. “But this observation was dismissed and largely forgotten due to the complexity of lipid biochemistry."

Further research revealed the fat deposits on the brains of nine Alzheimer's victims were triglycerides enriched with specific fatty acids, which can also be found in most animal fats and vegetable oils.

"We discovered that these fatty acids are produced by the brain, that they build up slowly with normal aging, but that the process is accelerated significantly in the presence of genes that predispose to Alzheimer's disease," said Fernandes.

In animal experiments, the researchers found that the fatty acids occur very early in life, correspnding in human years to the early twenties.

Cause or consequence?

Therefore, we think that the build-up of fatty acids is not a consequence but rather a cause or accelerator of the disease," Fernandes said.

If it turns out that these fat deposits are a significant contributor to Alzheimer's, the researchers say it would be a huge breakthrough. That's because there are existing drugs that inhibit the enzyme that produces these fatty acids.

The research team concludes these molecules, which are currently being tested for metabolic diseases such as obesity, could be effective in treating Alzheimer's disease.

"We succeeded in preventing these fatty acids from building up in the brains of mice predisposed to the disease. The impact of this treatment on all the aspects of the disease is not yet known, but it significantly increased stem cell activity," Fernandes said. "This is very promising because stem cells play an important role in learning, memory and regeneration."

The researchers say their discovery also supports the argument that Alzheimer's disease is a metabolic brain disease, almost like obesity or diabetes. They say it could lead to an entirely new approach to treatment.

Doctors in the UK treating cognitive decline recently made a startling discovery: their patients are getting younger.

Alzheimer's disease and other types of dementia usually show up when people are in their 60s, but doctors providing information for the Young Dementia UK charity say they have begun to treat patients in their 40s and 50s.

Researchers at Bournemouth University believe “modern life” may be mostly to blame. They studied adults in 21 Western countries and found that the problem was most severe in the U.S. They believe that environmental problems like pollution and pesticides could be at fault.

Deaths on the rise

At the same time, deaths resulting from neurological disease are up significantly in adults aged 55-74. For adults 75 and older, the rate has almost doubled in every Western country in just the last 20 years.

In the U.S., neurological disease deaths in men over 75 have nearly tripled and have increased even more in women. For the first time since records began, more elderly American women died of brain disease than cancer.

“The rate of increase in such a short time suggests a silent or even a hidden epidemic, in which environmental factors must play a major part, not just aging," said Colin Pritchard, a professor at Bournemouth University, who led the study. “Modern living produces multi-interactional environmental pollution but the changes in human morbidity, including neurological disease is remarkable and points to environmental influences.”

Hidden epidemic

As a result of the “hidden epidemic,” Prichard says health services are being swamped. He also says neurological diseases are becoming more common on a relative basis because many physical diseases are becoming less common. He does not that there is one big difference, though.

“Crucially it is not just because people are living longer to get diseases they previously would not have lived long enough to develop but older people are developing neurological disease more than ever before,” he said.

Why? Because the world is a very different place, he says.

“The environmental changes in the last 20 years have seen increases in the human environment of petro-chemicals – air transport- quadrupling of motor vehicles, insecticides and rises in background electro-magnetic-field, and so on,” Pritchard said.

With the huge Baby Boom population getting older, its members are naturally drawn to products that promote youth and vitality and slow physical and cognitive decline.

As such, the MIND diet is growing in popularity with this group. Researchers at Rush University Medical Center have found that sticking closely to the food included on the MIND diet may slow natural cognitive decline among aging adults, even when the person is not at risk of developing Alzheimer's disease.

Previously, the research team established that the MIND diet may reduce a person's risk of developing Alzheimer's disease.

This new research shows that older adults who followed the MIND diet faithfully showed an equivalent of being 7.5 years younger cognitively than those who followed the diet least.

The MIND diet

So, what's included in the MIND diet? The ingredients should be familiar since it is a rough combination of the Mediterranean and DASH diets. There are ten things you eat and five things you avoid.

The things you eat include at least three servings of whole grains, a green leafy vegetable, and one other vegetable every day -- along with a glass of wine. Followers of the diet also snack most days on nuts, have beans every other day or so, eat poultry and berries at least twice a week, and fish at least once a week.

As for the things to avoid, limit consumption of butter, sweets, pastries, whole fat cheese, and fried or fast food. Followers of the diet should have less than a serving a week for any of these products.

Berries – the only fruit specifically to be included in the MIND diet – are especially important.

"Blueberries are one of the more potent foods in terms of protecting the brain," said Martha Clare Morris, a nutritional epidemiologist and member of the research team. “Strawberries also have performed well in past studies of the effect of food on cognitive function.”

Scientifically proven

To reach its conclusions, the research team assembled 960 older adults who were completely free of dementia and evaluated their cognitive change over nearly five years. The participants averaged 81.4 years in age.

During the study, the participants were closely followed, receiving yearly standardized testing for cognitive ability in five areas - episodic memory, working memory, semantic memory, visuospatial ability, and perceptual speed.

The researchers were able to closely follow their subjects' diet, comparing participants' reported adherence to the MIND diet with changes in their cognitive abilities as measured by the tests.

"The MIND diet modifies the Mediterranean and DASH diets to highlight the foods and nutrients shown through the scientific literature to be associated with dementia prevention." Morris said. "There is still a great deal of study we need to do in this area, and I expect that we'll make further modifications as the science on diet and the brain advances."

Morris says the MIND diet can pay huge dividends for Boomers, since she says it can not only reduce the risk of Alzheimer's disease but slow natural cognitive decline as well. Delaying dementia's onset by just five years, she says, can reduce the cost and prevalence by nearly half.

Alzheimer’s and diabetes are two diseases that are becoming more and more widespread, even though they are very different from one another. 

Now however, researchers think they could have a common link.

Type 2 diabetes cases are on the rise, in part because of the huge increase in obesity – a major risk factor for the condition. Alzheimer’s cases are increasing, in large part because of the huge Baby Boom generation getting older. Age is a major risk factor for that illness.

An Iowa State University study, published in the Journal of the American Medical Association Neurology, found a strong association between insulin resistance and memory function decline, which is a dominant symptom of Alzheimer’s disease.

In May, researchers at Washington University at St. Louis reached a similar conclusion. They found that elevated sugar levels in the blood, which is a halmark of diabetes, can increase levels of amyloid beta, which shows up in brain plaques in Alzheimer's patients.

According to Auriel Willette, a research scientist in the Department of Food Science and Human Nutrition at Iowa State, insulin resistance is common in people who are obese, pre-diabetic, or have type 2 diabetes.

Brain scans

To explore a possible link, Willette and co-author Barbara Bendlin, of the Wisconsin Alzheimer’s Institute, closely examined brain scans in 150 late middle-aged adults. Each of them were at risk for Alzheimer’s disease, but had shown no sign of memory loss.

What the researchers were looking for was evidence that people with higher levels of insulin resistance used less blood sugar in areas of the brain most susceptible to Alzheimer’s. If that were the case, they theorized, the brain would have less energy to carry out its cognitive functions.

“If you don’t have as much fuel, you’re not going to be as adept at remembering something or doing something,” Willette said. “This is important with Alzheimer’s disease, because over the course of the disease there is a progressive decrease in the amount of blood sugar used in certain brain regions. Those regions end up using less and less.”

The area of focus was the medial temporal lobe, specifically the hippocampus. That's a region of the brain critical for learning new things and sending information to long-term memory. Willette says it's one of the most affected parts of the brain when someone develops Alzheimer's.

Huge step toward prevention

If there is a link between insulin resistance and Alzheimer’s disease, that could be a huge step toward prevention. But Willette says difficulty regulating blood sugar may impact cognitive function at any age, not just those at risk of Alzheimer's. That means young people who are obese or who are developing insulin resistance could face cognitive impairment at an early age.

The first step, however, is testing for insulin resistance in obese patients and taking corrective action through improved nutrition and moderate exercise.

“We are terrible at adjusting our behavior based on what might happen in the future,” Willette said. “That’s why people need to know that insulin resistance or related problems with metabolism can have an effect in the here and now on how they think, and it’s important to treat.”

He says even people with mild or moderate insulin resistance who don’t have type 2 diabetes might have an increased risk for Alzheimer’s disease because they’re showing many of the same sorts of brain and memory relationships.

Understanding the progression of cognitive decline and how it relates to insulin resistance will take additional research. Willette says following those who are at-risk through the different stages of dementia and Alzheimer’s will offer insight as to what happens as their cognitive function declines.

The Alzheimer's Association International Conference, an annual event held in Washington, DC, is usually marked by cautious optimism as pharmaceutical companies and health researchers report on their latest efforts to treat the memory-robbing disease.

This year has been no exception. While there have been no breakthroughs reported, there are a number of hopeful advances.

Solanezumab

Drug company Eli Lily reported that its new drug, solanezumab, might be able to slow the onset of Alzheimer's in the early stages of the disease. According to researchers, the drug can slow down the disease by about 33%.

Solanezumab works by attacking amyloid that builds up in the brain, which is believed to be a major contributor to Alzheimer's. Eli Lily says it plans to launch a new trial of the drug early next year. That trial, it says, should yield more information about the drug's efficacy.

Nuedexta

In another development, Avanir Pharmaceuticals disclosed its findings from the dementia/Alzheimer's disease cohort of the PRISM II study, a phase IV study evaluating the safety and effectiveness of Nuedexta in treating Alzheimer's paients.

Specifically, it treats pseudobulbar affect (PBA) in patients with dementia, as well as stroke and traumatic brain injury (TBI). PBA is a condition characterized by sudden and uncontrollable outbursts of laughing and/or crying resulting from certain neurologic diseases or brain injury.

The study concluded that a patient taking Nuedexta had no loss of effectiveness if they were also taking any anti-depressants.

Non-drug intervention

Researchers also reported positive results of three new randomized controlled trials of aerobic exercise in Alzheimer's disease, vascular cognitive impairment (VCI), and mild cognitive impairment (MCI).

The results provide hope that there may soon be a way that people with dementia can prolong their independence and improve their quality of life. The researchers said they found regular physical activity can reduce the risk of cognitive decline, and maybe even reduce the risk of Alzheimer's disease and other dementias.

It reflects similar findings that lifestyle changes can not only help people improve their physical health, but their mental health too.

The latest research suggests physical exercise can improve cognition while reducing symptoms in people with Alzheimer's by positively impacting the physical changes in the brain caused by the disease. Maria Carrillo, Alzheimer's Association Chief Science Officer, says this research is important because it highlights the potential value of non-drug therapies for Alzheimer's disease and other dementias.

“It reminds us that research ought to adamantly pursue combination and multi-modal approaches to Alzheimer's therapy and prevention," she said.

It has long been assumed that the combination of Alzheimer's disease and an aging Baby Boom generation will spell trouble. A recent study that was submitted at the Alzheimer's Association International Conference confirms that it will be pretty bad.

The report projects that 28 million Boomers – Americans born between 1946 and 1964 – will develop Alzheimer's at some point. Researchers predict that the cost of treating them will consume nearly 25% of all Medicare spending by 2040.

The report starts with the assumption that there will be no significant advancements in Alzheimer's treatment between now and then. Today, Alzheimer's remains a slowly developing disease that robs its victims of their memory before it is ultimately fatal. There is no known cure.

$11 billion to $328 billion

If nothing is done by 2020, the projected Medicare costs of caring for Baby Boomers with Alzheimer's is projected to be $11.86 billion in 2014 dollars, making up 2.1% of total Medicare spending. By 2040, when Boomers are aged 76-94, the projected Medicare costs are expected to be $328.15 billion in 2014 dollars.

"The risk of Alzheimer's increases with age, and as baby boomers get older, the number of people developing the disease will rise to levels far beyond anything we've ever seen before," said Keith Fargo, Alzheimer's Association Director of Scientific Programs & Outreach.

It's unlikely that medical research will stand still as this disease ravages a generation. Fargo says there is a pipeline of experimental therapies that have the potential to delay the onset of Alzheimer's and perhaps even prevent the disease. Many will get an airing at the association's conference this week in Washington, DC.

Promising developments

In fact, there have been a number of developments in the area of Alzheimer's research in the last few months. One of the more promising ones was revealed in October, when researchers said a novel and complex treatment had restored memory function in 9 out of 10 participants.

The study, conducted jointly by the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging, is the first to suggest that memory loss in patients may be reversed, and that improvement can be lasting.

The treatment consists of a 36-point therapeutic program involving comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific drugs and vitamins, and many additional steps that affect brain chemistry.

As we reported just last week, scientists in Texas have isolated a biomarker that may help doctors predict who will get Alzheimer's, allowing for early intervention.

Financial commitment 

Fargo points to recent advances in the treatment of HIV, cancer, and heart disease, saying the same financial commitment made to battling those deadly diseases is needed to tame Alzheimer's disease.

"Alzheimer's is extremely underfunded compared to the magnitude of the problem,” Fargo said. “If we're going to change the current trajectory of the disease, we need consistent and meaningful investments in research from the federal government to ensure a more robust pipeline."  

There is no conclusive test that can predict who will develop Alzheimer's disease as they age. However, it is information doctors would like to know, since it would allow earlier treatment and, perhaps, a delay in the onset of the fatal condition.

Researchers in the field are constantly looking for biomarkers that could offer a more complete picture of who is most at risk. They think they may have identified one in amnestic mild cognitive impairment (aMCI).

Researchers at the Center for BrainHealth at The University of Texas at Dallas have noticed that people with aMCI appear to be at twice the risk of developing Azheimer's disease when compared to others in their age group.

In findings published in the Journal of Alzheimer's Disease, researchers identify a specific variation in brain waves of people with aMCI. Specifically, they think a delayed neural activity in aMCI patients that shows up in a word-finding task may indicate an early dysfunction that points to the progression of Alzheimer's disease.

One of the main symptoms of Alzheimer's disease is the inability to retain new memories about recent conversations, events, or upcoming appointments.

Specific type of impairment

While mild cognitive impairment (MCI) is the recognized clinical state between healthy aging and Alzheimer's disease, aMCI is a specific type of impairment marked by deficits in episodic memory.

"This is a promising start at looking at a group of MCI patients. The long-term goal is whether this can be applied to individual patients one day," said study principal investigator John Hart.

If the method proves reliable, it could provide a more affordable and non-invasive alternative to other available methods, such as MRI or a spinal tap, to measure neural responses.

Examining spinal fluid

Researchers at Washington University School of Medicine in St. Louis have been studying brain scans and looking for biomarkers that could help with earlier diagnosis of Alzheimer's disease. In this study, scientists have found that changes in the spinal fluid during middle age may help doctors identify people at risk of developing Alzheimer's disease later in life.

"It's too early to use these biomarkers to definitively predict whether individual patients will develop Alzheimer's disease, but we're working toward that goal," said senior author Anne Fagan, PhD, a professor of neurology. "One day, we hope to use such measures to identify and treat people years before memory loss and other cognitive problems become apparent."

Early lifestyle changes can help

While there is currently no cure for Alzheimer's disease, the Alzheimer's Association recently released research suggesting lifestyle changes in middle age can reduce the risk of cognitive decline.

"The research on cognitive decline is still evolving," said Angela Geiger, who is the chief strategy officer of the Alzheimer's Association. "But there are actions people can take.”

For example, certain healthy behaviors known to combat cancer, cardiovascular disease, and diabetes may also reduce the risk of cognitive decline. These healthy behaviors include staying mentally active, engaging in regular physical activity, and eating a heart-healthy diet that benefits your body and your brain.

“There is also some evidence people may benefit from staying socially engaged with friends, family and the community," she said.

Researchers searching for new treatments for Alzheimer's disease recently made a startling observation.

They found that people with a genetic predisposition to high blood pressure also had a lower risk for Alzheimer's, a fatal condition that robs its victims of their memory.

That seemed counter-intuitive until they closely. The people with the genetic link to hypertension but who weren't getting Alzheimer's were being treated for their high blood pressure.

"It's likely that this protective effect is coming from antihypertensive drugs," said study co-author John Kauwe, an associate professor of biology at Brigham Young University (BYU). "These drugs are already FDA approved. We need to take a serious look at them for Alzheimer's prevention."

Researchers from around the world worked on the study, which examined genetic data from 17,008 people with Alzheimer's and 37,154 people free of the disease.

Looking for causal relationships

The research team was actually looking for something else – links between Alzheimer's disease and health conditions like diabetes, obesity, and high cholesterol. Specifically, they were looking for links to conditions that could be modified, like high blood pressure. But the assumption going into the project was that these modifiable conditions might be a contributor to Alzheimer's risk.

Amazingly, the strongest correlation that emerged was a “significant” association between higher systolic blood pressure and reduced Alzheimer's risk.

"Our results are the opposite of what people might think," said fellow co-author Paul Crane, a University of Washington associate professor of internal medicine. "It may be that high blood pressure is protective, or it may be that something that people with high blood pressure are exposed to more often, such as antihypertensive medication, is protecting them from Alzheimer's disease."

Role of ACE inhibitors

As we reported back in 2007, the scientific community has suspected that a certain class of hypertension drug might also help protect against Alzheimer's disease. Wake Forest University researchers made the case that a class of hypertension drugs known as ACE inhibitors might help reduce the inflammation that could contribute to Alzheimers disease.

The study found a link between taking centrally active ACE inhibitors and lower rates of mental decline as measured by the Modified Mini-Mental State Exam, a test that evaluates memory, language, abstract reasoning and other cognitive functions.

For each year that participants were exposed to ACE inhibitors that cross the blood brain barrier, the decline in test results was 50% lower than the decline in people taking other kinds of high blood pressure pills.

The results are not conclusive and this story is published only as general information. It is not medical advice and no one should make any decisions based on general news publications. Only your doctor can advise you about medications and treatments. 

Could be significant

The findings coud be significant since the global population is rapidly aging. Worldwide, about 44 million people have dementia, a group of brain degeneration disorders characterized by an irreversible decline in memory, communication, and other cognitive functions. Dementia mainly affects older people, and because people are living longer, experts estimate that more than 135 million people will have dementia by 2050.

Alzheimer's is the most common form of dementia, which accounts for 60% to 70% of cases. The earliest sign of Alzheimer's is often increasing forgetfulness. As the disease progresses, affected individuals gradually lose the ability to look after themselves, they may become anxious or aggressive, and they may have difficulty recognizing friends and relatives. 

Diagnosing Alzheimer’s disease and other neurodegenerative disorders may be easier in the future. A new study suggests that digitally mapping the brains of older people may help doctors detect anomalies and treat conditions much more quickly.

Doctors currently use MRI’s of healthy brains to compare individual cases and make diagnoses. The problem is that most of these MRI’s are of young or middle-aged brains. Diseases and disorders like Alzheimer’s primarily affect people who are older, so many of the MRI’s do not accurately depict what happens in our brains as we age.

Mapping the elderly brain

To remedy this, researchers from the University of Edinburgh created a detailed atlas of an aged human brain. The atlas was created from scans of over 130 people who were 60 years of age or older.

After creating the atlas, the research team compared brain scans of healthy, older brains and the brains of patients that had been diagnosed with Alzheimer’s disease. The atlas was able to locate areas in the brain where brain tissue was deteriorating, which can be an early sign of Alzheimer’s if caught in the early stages.

Earlier Diagnoses

“We’re absolutely delighted with these preliminary results and that our brain MRI atlases may be used to support earlier diagnoses of diseases such as Alzheimer’s. Earlier diagnoses are currently our strongest defense against these devastating diseases and, while our work is preliminary and ongoing, digital brain atlases are likely to be at the core of this defense,” said Dr. David Alexander Dickie, who is the first author of the study and a researcher at The University of Edinburgh’s Brain Research Imaging Center.

While researchers have had a great measure of success with their atlases, they are always looking for more data to make them more precise. They urge brain imaging centers to continue collecting scans of brains of people of all ages so that they can create large brain image banks to work from.

The full study is published in the journal PLOS ONE. 

For years doctors have advised older adults to remain physically and mentally active, to reduce the likelihood of dementia or Alzheimer’s disease.

It's still good advice, researchers say, but if you have the underlying markers for the disease, there are limits to its effectiveness.

“While a lifelong history of physical and mental activity may support better memory and thinking performance, this relationship may possibly be separate from any protection against the markers of Alzheimer’s disease in the brain,” said study author Keith A. Johnson, MD, with Harvard Medical School and Massachusetts General Hospital in Boston.

The study, published in the journal Neurology, followed older adults who had different levels of lifelong physical and mental activity. The most active engaged in things like bike riding, dancing, walking and gardening and mentally stimulating activities such as crosswords and reading. Make no mistake, those activities help.

Significantly higher IQs

The study participants took tests of their thinking and mental abilities. Results showed that participants who took part in stimulating cognitive activities had significantly higher IQ and better cognitive performance compared those who did not take part in mentally stimulating activities very often.

But there was no relationship between frequent mental or physical activity and any of the markers of Alzheimer’s disease in the brain.

“This suggests that sustaining a lifetime of intellectual engagement may help preserve cognitive function into old age,” said Johnson. “In addition, our findings should not discourage people from engaging in physically and mentally stimulating activities, as they have been shown in numerous studies to generally offer many brain benefits.”

In fact, the National Institute on Aging, which partially funded the study, says scientists continue to study other non-genetic risk factors for Alzheimer's, and continue to stress the importance of both physical and mental stimulation, along with social engagement and a nutritious diet, to delay the onset of the disease.

Other possible links

The Institute, which is part of the National Institutes of Health (NIH), says scientists are also investigating associations between cognitive decline and heart disease, high blood pressure, diabetes, and obesity.

“Understanding these relationships and testing them in clinical trials will help us understand whether reducing risk factors for these diseases may help with Alzheimer's as well,” the agency says on its website.

The Alzheimer's Association, which also funded the Harvard study, still stresses that people can reduce their risk of cognitive decline by maintaining a healthy lifestyle.

"The research on cognitive decline is still evolving," said Angela Geiger, chief strategy officer, Alzheimer's Association. "But there are actions people can take. Certain healthy behaviors known to combat cancer, cardiovascular disease and diabetes may also reduce the risk of cognitive decline.”

And those activities, says Geiger, include staying mentally active, engaging in regular physical activity and eating a heart-healthy diet that benefits both body and brain. She says there is also some evidence people may benefit from staying socially engaged with friends, family and the community.

Two studies published in the Journal of the American Medical Association today focus on the presence of plaque amyloid in the brain of adults as an early warning of Alzheimer's disease.

The studies analyzed adults of all ages and included those with some dementia and those who showed no signs of cognitive impairment. The results may help diagnose the progressive and fatal disease much earlier than is now possible.

The findings have added importance because Alzheimer disease (AD) is the most common cause of dementia. It affected about 25 million people worldwide in 2010 but that number is expected to double by 2030 because of longer life expectancy.

In one study researchers from the Netherlands measured the presence of amyloid in people with normal memory function, subjective cognitive impairment (SCI) and mild cognitive impairment (MCI).

Presence of amyloid is key indicator

The researchers found the prevalence of amyloid pathology in all three groups of adults age 50 to 90. Those with normal memory had the least while those who already showed some mild cognitive loss had the most.

Those who carried a certain gene, called apolipoprotein E, had two to three times the presence of anyloid as those who didn't have the gene.

The researchers believe this study has several implications for understanding how Alzheimer's disease develops.

“The observation that key risk factors for AD-type dementia are also risk factors for amyloid positivity in cognitively normal persons provides further evidence for the hypothesis that amyloid positivity in these individuals reflects early AD,” the authors write.

As early as age 30

They also maintain their findings show that AD pathology can start as early as age 30. This means there could be a 20- to 30-year interval between the first signs of amyloid positivity and dementia, suggesting that there is a large window of opportunity to start preventive treatments.

The second study, conducted by another group of Dutch researchers, looks at ways to more narrowly interpret the clinical significance of positron emission tomography (PET), used to find amyloid positivity in the brain. Specifically, the researchers focused on ways to better understand the prevalence of amyloid positivity across different types of dementia and how this is associated with demographic, genetic, and cognitive factors.

They studied people diagnosed with Alzheimer's as well as those who had other types of dementia. Those diagnosed with Alzheimer's had an average prevalence of amyloid positivity of 88%, that actually decreased with age unless they carried the apolipoprotein E gene. Those sufferings from non-AD dementia showed an increase in amyloid as they aged.

Implications

The researchers conclude that the early signs of Alzheimer's might be easier to find in younger adults, even before they start to show symptoms of cognitive impairment.

There is no cure for Alzheimer's but there are treatments that doctors say can slow the progression of the disease.

The Alzheimer's Association says the Food and Drug Administration (FDA) has approved 2 types of drugs to treat the symptoms of memory loss and reasoning. There are also treatments available to address changes in behavior brought on by Alzheimer's disease.

With rising obesity, America faces an increased number of type 2 diabetes cases. With an aging Baby Boom generation, the country is bracing for an increase in Alzheimer's disease.

Could the two be related?

Previous studies have hinted at such a link. But researchers at Washington University School of Medicine in St. Louis say they have nailed down the connection.

Their study, using mice, found that elevated glucose in the blood – a primary consequence of diabetes -- can rapidly increase levels of amyloid beta, which shows up in brain plaques in Alzheimer’s patients. The buildup of these plaques is believed to be what brings on the memory loss that Alzheimer’s causes in the brain.

Could lead to new treatments

“Our results suggest that diabetes, or other conditions that make it hard to control blood sugar levels, can have harmful effects on brain function and exacerbate neurological conditions such as Alzheimer’s disease,” said lead author Shannon Macauley, a postdoctoral research scholar. “The link we’ve discovered could lead us to future treatment targets that reduce these effects.”

There are two types of diabetes, type 1 mostly hereditary and the other, type 2, usually brought on by lifestyle factors, such as being overweight or obese. In both types the patient is unable to control glucose, or sugar levels in their blood.

Diabetes patients usually take insulin or other medication to keep their blood sugar where it is supposed to be.

So what does blood sugar have to do with Alzheimer's? To explore the linkage the researchers fed glucose to mice with an Alzheimer's-like condition.

The experiment

If the mice did not have the amyloid plaques in the brains, doubling their blood glucose levels increased amyloid beta levels in the brain by 20%. When the scientists repeated the experiment in older mice that already had developed brain plaques, amyloid beta levels rose by 40%.

When blood glucose levels spiked, it increased brain activity that helped produce amyloid beta.

“This observation opens up a new avenue of exploration for how Alzheimer’s disease develops in the brain as well as offers a new therapeutic target for the treatment of this devastating neurologic disorder,” Macauley said.

Speeds up aging

Meanwhile, researchers at the University of Pittsburgh Graduate School of Public Health say they have found another link between diabetes and diminished memory function. They studied the brains of people with type 1 diabetes and found these brains aged faster, correlating with slower information processing.

Among the middle-aged test subjects who underwent an MRI, 33% of those with type 1 diabetes showed signs of damage to the brain's white matter. Only 7% of subjects who were not diabetic showed similar damage.

The researchers suggest middle-aged patients with type 1 diabetes should be screened for cognitive difficulties. If cognitive issues are progressive, they say these changes could influence a patients ability to manage his or her diabetes.  

Over the last 5 years or so researchers have made tantalizing progress against the scourge of Alzheimer's disease, but the developments have yet to get to the final phase of testing.

Then suddenly last week a drug from pharmaceutical giant Biogen Idec grabbed the attention of the scientific world. It also got the attention of a perhaps harder-to-impress group – Wall Street traders. Biogen stock surge nearly 10% in a single day.

It was all because the company announced that a Phase 1b study of one of its drugs, aducanumab, demonstrated that it was safe for people to take. The reason people would take the drug is it is believed to be a powerful weapon against Alzheimer's disease.

Reduces plaque

Previous studies have show that treatment with aducanumab reduced the amount of amyloid plaque in the brain. Amyloid plaque is believed to be largely responsible for the cognitive decline associated with Alzheimer's.

The company points to a series of exploratory analyses, showing a dose-dependent, statistically significant effect of slowing clinical decline was observed on the Mini Mental State Examination (MMSE) and Clinical Dementia Rating (CDR) scales.

“This is the first time an investigational drug for Alzheimer’s disease has demonstrated a statistically significant reduction on amyloid plaque as well as a statistically significant slowing of clinical impairment in patients with prodromal or mild disease,” said Dr. Alfred Sandrock, group senior vice president and chief medical officer at Biogen. “Based on these results, we are advancing the aducanumab clinical program to Phase 3 with plans to initiate enrollment later this year.”

Phase 3 trial

That last sentence is key. During a Phase 3 trial, the drug or treatment is given to large groups of people to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely. It is the last step before applying to the U.S. Food and Drug Administration (FDA) for approval to be marketed in the U.S.

According to the Wall Street Journal, industry analysts were excited because brain imaging scans have shown reductions in plaque, corresponding to clinical improvements. The paper quotes Christopher Raymond, analyst for Robert Baird, as saying “these data are more impressive than anything we have seen in Alzheimer's disease.”

Biogen says its Phase 3 trial, testing the efficacy of the drug, will include more than 1,000 patients.

Hopeful news for Boomers?

It's significant any time there is a promising development in treatment for a chronic disease that is ultimately fatal. Because of a population trend, this development might prove to be particularly significant.

One of the major Alzheimer's risk factors is age. With the huge Baby Boom generation now entering its senior years, the risk of a surge in Alzheimer's cases is growing.

A report (PDF) last month by the Alzheimer's Association projected the cost of treating the disease in the U.S. could swell to $1 trillion a year by 2050.

In 2010, the World Health Organization (WHO) estimated that 25 million individuals worldwide were living with Alzheimer's. Researchers believe changes to the brain typically begin years prior to the symptoms that lead to a clinical diagnosis.  

The twin tragedies of Alzheimer's disease are that it is always fatal and, before the patient dies, they lose all memory function.

Researchers at UCLA are convinced they are on the cusp of a breakthrough in which memory loss can not only be slowed but lost memories restored in patients in the early stages of Alzheimer's disease.

We reported in October on a small study conducted jointly by the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging. It was the first to suggest that memory loss in patients may be reversed, and that improvement can be lasting. Since then there has been nothing to temper that optimism.

The latest research focuses on where memories are actually stored in the brain. The assumption has always been that these memories are stored at the synapses -- the connections between brain cells, or neurons -- which are destroyed by Alzheimer's disease. The latest research provides evidence contradicting that assumption.

Radical idea

"Long-term memory is not stored at the synapse," said David Glanzman, a senior author of the study, and a UCLA professor of integrative biology and physiology and of neurobiology. "That's a radical idea, but that's where the evidence leads. The nervous system appears to be able to regenerate lost synaptic connections. If you can restore the synaptic connections, the memory will come back. It won't be easy, but I believe it's possible."

The UCLA team came to this conclusion, oddly enough, by studying snails. From that study the scientists conclude that the body may be able to grow new synaptic connections. It all has to do with protein substances created in the body naturally and which are tied to memory formation.

As long-term memories are formed, the brain creates new proteins that are involved in making new synapses. If something happens to disrupt this process – for example by a concussion or other injury -- the proteins may not be synthesized and long-term memories cannot form. This is why people cannot remember what happened moments before a concussion.

Role of proteins

"If you train an animal on a task, inhibit its ability to produce proteins immediately after training, and then test it 24 hours later, the animal doesn't remember the training," Glanzman said. "However, if you train an animal, wait 24 hours, and then inject a protein synthesis inhibitor in its brain, the animal shows perfectly good memory 24 hours later.”

In other words, once memories are formed, if you temporarily disrupt protein synthesis, it doesn't affect long-term memory. Glanzman says that's true for the brains of both snails and humans and explains why people's older memories usually survive a concussion.

Stored in neurons?

But what does this have to do with Alzheimer's disease? Glanzman says he believes his team has shown that memories are not stored in synapses but elsewhere in the brain – most likely in neurons. So when damaged synapses are restored, there would be restored access to those memories.

Glanzman said the research could have significant implications for people with early-stage Alzheimer's disease. Specifically, just because the disease is known to destroy synapses in the brain doesn't mean that memories are destroyed.

"As long as the neurons are still alive, the memory will still be there, which means you may be able to recover some of the lost memories in the early stages of Alzheimer's," he said.

But in advanced stages of Alzheimer's neurons die. If Glanzman is correct that memories reside in neurons, that likely means the memories cannot be restored once the neurons are destroyed.

There is a new urgency to Alzheimer's research since the large Baby Boom population is entering the period of highest risk. While Alzheimer's is not a normal part of aging the Alzheimer's Association says people age 65 and older are at the highest risk.

As people get older they often assume that losing a step mentally is just part of the aging process. Having a “senior moment” might be just that, or it might be the sign of something else.

People who are concerned they may be experiencing memory issues need to talk about it with their doctor, but most don't. University of Michigan (UM) researchers and their colleagues conclude that more than half of seniors with signs of memory loss never see a doctor about it.

The Michigan findings suggest that as many as 1.8 million Americans over the age of 70 with dementia have not been evaluated for cognitive symptoms by a medical provider. Getting help, the researchers say, could lead to treatments that can improve memory function, or slow down its decline.

Not getting needed care

"Early evaluation and identification of people with dementia may help them receive care earlier," said study author Vikas Kotagal.

It can also help families make plans for care and watch for future problems that can occur.

“In some instances, these interventions could substantially improve the person's quality of life," Kotagal said.

Why?

The study failed to find out why more seniors with with onset of memory problems don't get help but it made some interesting observations.

Married seniors were more than twice as likely to get cognitive exams as people who were not married. Kotagal believes that's because a spouse will be less hesitant to bring up the subject than an adult child would be. And a spouse observes the patient on a daily basis, while an offspring might not.

"Another possibility could be that unmarried elderly people may be more reluctant to share their concerns with their doctor if they are worried about the impact it could have on their independence," Kotagal said.

Alzheimer's disease

Not all dementia is related to Alzheimer's disease but a lot of it is. Dementia is a condition caused by damage to neurons in the brain that interfere with memory function.

With Alzheimer's, the neuron damage is so severe it eventually interferes with life functions and the patient dies. According to the Alzheimer's Association, Alzheimer's makes up as many as 80% of dementia cases.

Warning signs

According to the National Institute on Aging, here are the warning signs seniors and their caregivers should be aware of:

• Asking the same question or repeating the same story over and over again
• Forgetting how to do activities that were previously routine, such as cooking, making repairs, or playing cards
• Losing the ability to handle money or balance a checkbook
• Getting lost in familiar surroundings or misplacing household objects
• Neglecting to bathe or wearing the same clothes over and over again and often insisting that he or she has bathed or that his or her clothes are still clean
• Relying on someone else, such as a spouse, to make decisions or answer questions he or she previously would have handled themselves.

In the meantime, Kotagal says both patients and their physicians should be more proactive on the issue. Doctors, he says, should more frequently recommend cognitive exams and patients should request them.

They reason they don't, Kotagal concludes, is that neither sees that much value in them. But the Michigan researchers say early intervention can help patients and lower societal costs.

Walnuts are a natural food and play a prominent role in the popular Mediterranean diet. Over the years health advocates have extolled their many health benefits.

Now, scientists in New York have completed an animal study that suggests another health benefit – reducing the risk, delaying the onset, slowing the progression of, or preventing Alzheimer's disease.

The research carried out by the Developmental Neuroscience Laboratory at the New York State Institute for Basic Research in Developmental Disabilities (IBR) found significant improvement in learning skills, memory, reducing anxiety, and motor development in mice fed a walnut-enriched diet.

The researchers think that might have something to do with the high antioxidant content found in walnuts. They speculate these antioxidants provided protection to the mouse brain, preventing the degeneration typically seen in Alzheimer's disease. Oxidative stress and inflammation are prominent features in this disease, which affects more than 5 million Americans.

Promising results

"These findings are very promising and help lay the groundwork for future human studies on walnuts and Alzheimer's disease – a disease for which there is no known cure," said lead researcher Dr. Abha Chauhan. "Our study adds to the growing body of research that demonstrates the protective effects of walnuts on cognitive functioning."

For the study the mice were fed dietary supplements with 6% to 9% walnuts, which is the equivalent of a human eating 1 to 1.5 ounces each day.

It's estimated that someone in the U.S. develops Alzheimer's disease every 67 seconds, and that number is expected to escalate rapidly as the Baby Boom generation ages. By 2050, health experts say the number of people 65 and older with Alzheimer's disease may nearly triple, from 5 million to as many as 16 million, creating new urgency to find treatments or a cure.

Walnuts and cancer

Walnuts are said to have other health and nutritional benefits, including reducing the risk of prostate and breast cancer. The American Institute for Cancer Research (AICR) says there are a few dozen studies investigating cancer and whole walnuts, with many more on the compounds they contain.

However, AICR says the current evidence is too limited to draw any conclusions about walnuts – or any nuts – and cancer risk.

Walnut's healthy effect on the heart is better documented. The National Institutes of Health (NIH) says in the last 2 decades a number of clinical studies have evaluated the effects of walnut consumption on cardio-vascular disease (CVD) risk factors.

According to NIH, walnuts can reduce low density lipoprotein cholesterol and blood pressure, both major risk factors for CVD.

Part of a healthy diet

“The effect of walnuts on multiple CVD targets over relatively short periods of time supports recommendations for their inclusion in a heart-healthy diet,” NIH says.

Walnuts have also been shown to be effective in weight control. They are a good source of fiber and make you feel full.

At the same time, you need to be prudent with your walnut consumption because they are loaded with calories. A tablespoon of chopped walnuts contains about 50 calories.

A cold sore is about as annoying as minor annoyances get. But it may be more than annoying. A new study finds that infection wih the herpes simplex virus increase the risk of Alzheimer's disease.

"Our results clearly show that there is a link between infections of herpes simplex virus and the risk of developing Alzheimer's disease. This also means that we have new opportunities to develop treatment forms to stop the disease," said Hugo Lövheim, a professor at Umeå University and one of the authors of the study, published in the journal Alzheimer’s & Dementia.

In recent years research has increasingly indicated that there is a possible connection between infection with a common herpes virus, herpes simplex virus type 1, and Alzheimer's disease. A majority of the population carries this virus.

After the first infection the body carries the virus throughout your lifetime, and it can reactivate now and then and cause mouth ulcers. The hypothesis which links the herpes virus and Alzheimer's disease is based on the notion that a weakened immune system among the elderly creates opportunities for the virus to spread further to the brain, starting the process which results in Alzheimer's disease.

Lövheim and a colleague, Fredrik Elgh, have confirmed this link in two large epidemiological studies.

In one study, the researchers show that a reactivated herpes infection doubled the risk of developing Alzheimer's disease. This study had 3,432 participants who were followed for 11.3 years on average.

In another study, 360 people with Alzheimer's disease were examined and compared to 360 others who had not developed dementia. The samples were taken on average 9.6 years before diagnosis. This study showed an approximately doubled risk of developing Alzheimer's disease if the person was a carrier of the herpes virus.

"Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer's disease," said Lövheim.

A small study of early Alzheimer's disease patients has produced stunning results. Researchers say a novel and complex treatment has restored memory function in 9 of the 10 participants.

The study, conducted jointly by the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging, is the first to suggest that memory loss in patients may be reversed, and that improvement can be lasting.

The treatment consists of a 36-point therapeutic program involving comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific drugs and vitamins, and multiple additional steps that affect brain chemistry.

Caveat

While this is very hopeful news, it comes with a rather large caveat. Dale Bredesen, author of the study, notes the very small size of the sample makes the results anecdotal. Still, it's impressive.

To prove whether or not researchers have finally unlocked the secret to turning back Alzheimer's, Bredesen says the treatment should be subjected to a large clinical trial. In the case of Alzheimer’s disease, Bredesen says there is not one drug that has been developed that stops or even slows the disease’s progression, and drugs have only had modest effects on symptoms.

“In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer’s at an aggregate cost of over $1 billion, without success,” he said.

Combination of treatments

While a combination of therapies has been used to control major chronic illnesses like cancer, the combination approach has never been applied to Alzheimer's. Bredesen says a broader-based therapeutics approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of the disease that eventually robs victims of their memory.

Though too small to be considered scientific proof, the UCLA-Buck Institute study achieved remarkable results. One patient had two years of progressive memory loss and was considering quitting her job, which involved analyzing data and writing reports. She got disoriented driving, and mixed up the names of her pets.

A second patient kept forgetting once-familiar faces at work, forgot his gym locker combination, and had to have his assistants constantly remind him of his work schedule.

A third patient's memory was so bad she used an iPad to record everything, then forgot her password. Her children noticed she commonly lost her train of thought in mid-sentence, and often asked them if they had carried out the tasks that she mistakenly thought she had asked them to do.

Improved memory function

Following the complex therapy, all 3 patients displayed improvement in their memories beginning within 3 to 6 months after the program’s start. Six patients who had to stop working or were struggling with their jobs at the time they joined the study were able to return to work or continue working with improved performance.

The only patient in the study who did not show improvement turned out to be in late stage Alzheimer's disease, suggesting the therapy is most effective for those whose cognitive impairment is diagnosed early.

There is nothing better to clear your head then being in the outdoors. It's one of the reasons gardening is so popular -- and the main reason that therapists are increasingly using gardening to help patients with dementia.

Horticulture therapy, as it's called, uses gardening activities in a therapeutic and rehab setting to improve the quality of life, possibly reducing costs for long-term, assisted living and dementia unit residents. The therapy has been shown to reduce pain, improve attention, lessen stress, and ease agitation, according Psychiatry Investigation, an academic journal. It may also lower the need for medication in some patients.

How to do it 

You want to make sure you create a space that is safe. You may need to build raised beds of different heights so people who are in a wheelchair can use the garden. Also remember that sometimes it is difficult for older people to bend over.

Try to make the garden as natural as possible. A fence or high walls can be perceived as closing in by some patients. It's best to cover them with shrubs or vines.

Make sure the garden is pretty easy to get to. You might have to make some signs. Pictures and words might help.

Unlocking doors and allowing people with dementia to come and go freely within the garden will encourage its use. One research study showed that propping open the doors to the garden doubled the number of times people used it independently.

Include shade areas that offer protection from the sun. Make a little place where patients can sit and relax. Be mindful of the type of plants you put in and don't use toxic plants or plants that can cause itching.

The surface should be as non-slip as possible; it's important for people who might not be so steady on their feet. Ponds and water features are wonderful but you have to be very careful how they are placed. Rails and ramps are good additions so that people with dementia can use the garden alone. After all, independence is so important when you have lost a big part of it and you are so dependent on others for many things.

Inside option

Another alternative is to plant a small garden inside, especially if you live in an area where the weather is not conducive to spending times outdoors. To be able to have a small space to see beautiful bright flowers and plants on a cold grey day will elevate everyone's spirit.

Don't worry if your garden is small or not yet filled with plants. It's better than watching TV, which is how far too many seniors spend their time in institutional settings. A garden is a great alternative and one that also gives a purpose. A garden is a pefect place to help stimulate memories with loved ones and staff. It welcomes interaction.

Two new research studies have shed new light on who will be afflicted with dementia, like Alzheimer's disease, and why. They join the growing body of research that is giving doctors better insight to the aging-related disease that robs seniors of their memory. It's of growing concern since the large Baby Boom generation is now entering old age and is at risk.

The first study, by researchers at the University of Exeter Medical School, links dementia with heavy alcohol consumption during middle age. It found that middle-aged adults with a history of problem drinking are more than twice as likely to suffer from severe memory impairment in later life.

"We already know there is an association between dementia risk and levels of current alcohol consumption – that understanding is based on asking older people how much they drink and then observing whether they develop problems,” said lead author Iain Lang. “But this is only one part of the puzzle and we know little about the consequences of alcohol consumption earlier in life.”

To find answers Lang and his team investigated the relatively unknown association between having a drinking problem at any point in life and experiencing problems with memory later in life.

"This is a public health issue that needs to be addressed,” Lang said. “More research is required to investigate the potential harms associated with alcohol consumption throughout life.”

Older people drinking more

The finding is particularly troubling in light of recent evidence that more middle-aged and elderly people are abusing alcohol. The National Council on Alcoholism and Drug Dependence says alcohol and prescription drug problems among adults 60 and older is one of the fastest growing health problems facing the country.

It says thousands of older people who need treatment for alcohol dependence aren't receiving it.

Meanwhile, an international study of 27,000 patients has established an unusual test to determine whether a patient is likely to develop dementia. The test measured how fast the subjects walked and answered a short series of questions. The slower the gait and the more wrong answers, the higher the risk of developing dementia.

Scientists at Albert Einstein College of Medicine, who conducted the study, said people who failed the test were twice as likely as others to develop dementia within 12 years.

Low-tech test

What makes the test important, the researchers say, is that it does not rely on sophisticated or expensive equipment, making it accessible to physicians in remote regions of the world. Testing relies on measuring gait speed and asking a few simple questions about a patient's cognitive abilities, both of which take just seconds.

"In many clinical and community settings, people don't have access to the sophisticated tests – biomarker assays, cognitive tests or neuroimaging studies – used to diagnose people at risk for developing dementia," said senior author Joe Verghese. "Our assessment method could enable many more people to learn if they're at risk for dementia, since it avoids the need for complex testing and doesn't require that the test be administered by a neurologist.

Early diagnosis, of course, is critical because it allows time to identify and possibly treat the underlying causes of the disease, which may delay or even prevent the onset of dementia in some cases.

The U.S. Centers for Disease Control and Prevention estimates that up to 5.3 million Americans—about 1 in 9 people age 65 and over – have Alzheimer's disease, the most common type of dementia. That number is expected to more than double by 2050 due to population aging.

Depression is rather common among seniors and so, unfortunately, is Alzheimer's disease. And now researchers say they have found a link between the two.

In fact, they say, late-life depression could become a major risk factor for developing Alzheimer’s faster than those who aren't depressed, according to research unveiled at the Society of Nuclear Medicine and Molecular Imaging’s 2014 Annual Meeting.

Depression has been previously proven to have its own neurodegenerative effects on the brain, but researchers say they have now found an undeniable connection between beta-amyloid in depressed elderly patients with cognitive deficits and advancement to Alzheimer’s disease. They were able to demonstrate this using molecular imaging data from a global dementia imaging database.

“Our results clearly indicate that mild cognitively impaired subjects with depressive symptoms suffer from elevated amyloid levels when compared with non-depressed individuals,” said the study’s principal scientist, Axel Rominger, MD, from the department of nuclear medicine at the University of Munich in Germany. “The combination of elevated amyloid levels and coexisting depressive symptoms constitute a patient population with a high risk for faster progression to Alzheimer’s disease.”

The finding could help patients make necessary lifestyle changes in an attempt to head off the deadly disease. 

“Therapeutic options for Alzheimer’s disease are still limited and therefore the identification and understanding of contributing risk factors that influence the disease are crucial in ongoing research as they offer the possibilities for future medical intervention,” said co-author and fellow researcher Matthias Brendel. 

Study details

The study involved 371 patients with mild cognitive impairment who underwent PET imaging with the radiotracer F-18 florbetapir and magnetic resonance imaging (MRI) chosen retrospectively from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database, which includes data from at least 55 research centers across the U.S. and Canada now readily available to more than 2,500 researchers worldwide.

Results showed that mild cognitive impaired patients with depressive symptoms had higher amyloid deposition than non-depressed controls as indicated by the binding of the radiotracer to amyloid particularly in the frontal cortex and the anterior and posterior cingulate gyrus of the brain, both involved in mood disorders such as depression.

Alzheimer’s disease is the most prevalent form of dementia. It is estimated that 44.4 million people are living with dementia worldwide. This number is expected to increase to approximately 75.6 million in 2030 and 135.5 million in 2050, according to 2013 data from the Alzheimer’s Disease International.

With millions of Americans already suffering from Alzheimer's disease and other forms of dementia and millions more approaching the age when they are most vulnerable, does it seem likely that a $30 nutritional supplement would do what some of the world's best scientists have been unable to do?

Of course not but that didn't stop i-Health, Inc. and Martek Biosciences Corporation from advertising that their BrainStrong Adult dietary supplement could improve adult memory and prevent cognitive decline.

The Federal Trade Commission charged that the advertising was deceptive and that the marketers falsely claimed they had clinical proof that BrainStrong Adult improves adult memory.

“Supplement marketers must ensure that adequate scientific proof supports their specific advertising claims,” said Jessica Rich, Director of the FTC’s Bureau of Consumer Protection. “When the results of a scientific study don’t match the hype, consumers are likely to be misled.”

$1 a day

Since at least March 2011, i-Health and Martek have sold BrainStrong Adult for about $30 for a 30-day supply at major retail stores, including CVS Pharmacy, Walmart, Walgreens, and Rite Aid; and online through drugstore.com and Amazon.com. They advertised the product – which contains the Omega-3 fatty acid DHA – on television, on Twitter, and at www.brainstrongdha.com.

In the television ad, a woman forgets why she walked into a room. Through a voice over, her dog tells the audience she is there to find her sunglasses, which are sitting on top of her head. Another voice over then asks, “Need a memory boost? Introducing BrainStrong…Clinically shown to improve adult memory.”

The FTC's proposed administrative settlement covers any dietary supplement, food, or drug promoted to prevent cognitive decline or improve memory, or containing DHA. It bars the companies from claiming that any such product prevents cognitive decline or improves memory in adults unless the claim is truthful and supported by human clinical testing.

The settlement also prohibits claims about the health benefits, performance, safety, or effectiveness of these products unless the claims are backed up by competent and reliable scientific evidence.

Finally, the companies cannot claim they have clinical proof to support their claims when they do not.

Estimates vary but the National Institute on Aging believes as many as 5.1 million Americans have Alzheimer's disease. This irreversible, progressive brain disease slowly destroys memory and thinking skills and eventually even the ability to carry out the simplest tasks.

As the Baby Boom generation enters old age there is concern that the number of people with this cognitive disease could surge, severely taxing the health care system.

While recent research has been promising, a cure is not on the horizon. However, an early warning system may be.

Neurologist Dr. David Geldmacher leads the University of Alabama at Birmingham (UAB) memory disorders program. He sees Alzheimer's patients on a daily basis. When he talks with the patients' caregivers, he says he invariably gets the question, “can this happen to me?”

Does it run in the family?

“It is very common for family members of a patient receiving a diagnosis of Alzheimer’s disease or other form of dementia to wonder about their own risk,” said Geldmacher.

Because of the persistent question Geldmacher began looking into ways to possibly predict whether someone will be affected by Alzheimer's disease or some other cognitive impairment. He's begun to prepare a personalized dementia risk assessment for people concerned about their risk for developing memory problems as they age.

As part of the assessment he compiles a family history and provides an in-depth memory history for the patient, cognitive testing and a baseline MRI scan. The results all go into risk predictor models.

From that, Geldmacher believes it will be possible to quantify the risk factors for Alzheimer's disease, as well as identify risk factors that, once reduced, can lessen the chances of developing the disease.

He says existing research has already established that negating one or more risk factors can reduce a patient's overall risk of getting Alzheimer’s disease.

Reducing the risk

“Our goal is to understand what risk factors are present in each individual and create a plan that best helps them reduce their risk and make appropriate plans for the future,” Geldmacher said.

Ideally, subjects would undergo the assessment when they are in their 50s and 60s and before they display any symptoms. The results should provide a risk prediction covering the next 20 years.

Not only that, Geldmacher believes that knowing the risks will allow – and motivate – people to take steps that can minimize the risk of serious memory loss.

The UAB clinic is currently setting up the assessment program. Participants will get two clinical visits with Geldmacher and his staff. The first will be to compile histories and conduct testing.

The second will be to go over a customized treatment plan, with instructions on how to access resources to achieve lifestyle changes and where to find supportive educational materials.

The two-visit assessment and treatment will cost about $1,000, which includes the MRI scan.

“It’s really for those who are worried about their cognitive health but do not currently have major memory issues,” Geldmacher said.

Blood test

UAB is not the only institution working on a treatment to predict Alzheimer's disease. Earlier this year researchers at Georgetown University Medical School said a simple blood test can predict with 90% accuracy whether someone will develop Alzheimer's.

If an analysis of the blood shows low levels of 10 specific blood fats, it's highly likely the patient will display dementia symptoms in the future.

"We do not know why all 10 of those lipids are lower in individuals who are predisposed to go on to cognitive impairment," said study author Dr. Howard Federoff.

But again, researchers believe having an early warning of impending Alzheimer's can help a patient make the lifestyle changes that can significantly delay its onset.

A new study finds that moderate physical activity may protect brain health and help prevent Alzheimer's disease.

The study of older adults at increased risk for Alzheimer's disease found that those who were more active had less shrinkage of the hippocampus – the brain region responsible for memory and spatial orientation that is attacked first in Alzheimer's disease.

Dr. J. Carson Smith, a kinesiology researcher in the University of Maryland School of Public Health who conducted the study, says that while all of us will lose some brain volume as we age, those with an increased genetic risk for Alzheimer's disease typically show greater hippocampal atrophy over time. The findings are published in the open-access journal Frontiers in Aging Neuroscience.

Delay cognitive decline

"The good news is that being physically active may offer protection from the neurodegeneration associated with genetic risk for Alzheimer's disease," Smith said. "We found that physical activity has the potential to preserve the volume of the hippocampus in those with increased risk for Alzheimer's disease, which means we can possibly delay cognitive decline and the onset of dementia symptoms in these individuals. Physical activity interventions may be especially potent and important for this group."

Smith and colleagues, including Dr. Stephen Rao from the Cleveland Clinic, tracked four groups of healthy older adults ages 65-89, who had normal cognitive abilities, over an 18-month period and measured the volume of their hippocampus (using structural magnetic resonance imaging, or MRI) at the beginning and end of that time period.

The groups were classified both for low or high Alzheimer's risk (based on the absence or presence of the apolipoprotein E epsilon 4 allele) and for low or high physical activity levels.

No other treatments as effective

Of all four groups studied, only those at high genetic risk for Alzheimer's who did not exercise experienced a decrease in hippocampal volume (3 percent) over the 18-month period. All other groups, including those at high risk for Alzheimer's but who were physically active, maintained the volume of their hippocampus.

"This is the first study to look at how physical activity may impact the loss of hippocampal volume in people at genetic risk for Alzheimer's disease," says Dr. Kirk Erickson, an associate professor of psychology at the University of Pittsburgh. "There are no other treatments shown to preserve hippocampal volume in those that may develop Alzheimer's disease. This study has tremendous implications for how we may intervene, prior to the development of any dementia symptoms, in older adults who are at increased genetic risk for Alzheimer's disease."

This may not be a test that anyone is very eager to take, but researchers at Georgetown University say they have developed a blood test that can predict with more than 90% accuracy whether a healthy person will develop Alzheimer's disease or other dementias within three years.

It's the first known test that can identify blood markers for Alzheimer's before symptoms begin to appear.

Although there is currently no cure for Alzheimer's, the Georgetown team says their test would give patients, their physicians and researchers a headstart at battling the disease.

"Our novel blood test offers the potential to identify people at risk for progressive cognitive decline and can change how patients, their families and treating physicians plan for and manage the disorder," said Howard J. Federoff, MD, PhD, professor of neurology and executive vice president for health sciences at Georgetown University Medical Center.

Described in Nature Medicine, the test identifies 10 lipids, or fats, in the blood that predict disease onset. It could be ready for use in clinical studies in as few as two years.

Federoff said the test offers "a window of opportunity for timely disease-modifying intervention" by giving an early warning that would allow new drugs and therapies, once they are developed, to slow or stop further development of the invariably fatal disease, which robs victims of their memory and intellectual faculties. 

"Biomarkers such as ours that define this asymptomatic period are critical for successful development and application of these therapeutics," he said.

A growing epidemic

There is no cure or effective treatment for Alzheimer's. Worldwide, about 35.6 million individuals have the disease and, according to the World Health Organization, the number will double every 20 years to 115 million by 2050.

"We consider our results a major step toward the commercialization of a preclinical disease biomarker test that could be useful for large-scale screening to identify at-risk individuals," Federoff said. "We're designing a clinical trial where we'll use this panel to identify people at high risk for Alzheimer's to test a therapeutic agent that might delay or prevent the emergence of the disease."

A generic antidepressant drug -- citalopram – has been found to relieve agitation significantly in a group of patients with Alzheimer's disease.

In lower doses than those tested, the drug -- sold under the brand names Celexa and Cipramil -- might be safer than antipsychotic drugs currently used to treat the condition, according to results of a clinical trial led by Johns Hopkins researchers that included seven other academic medical centers in the U. S. and Canada.

For the study, reported in the Feb. 19 issue of the Journal of the American Medical Association, Constantine Lyketsos, M.D., M.H.S., and his colleagues recruited 186 Alzheimer's patients who showed a collection of symptoms including emotional distress, excessive movement, aggression, disruptive irritability and disinhibition.

None experienced adequate symptom relief with non-medical therapies, and some experienced failed treatment with antipsychotic drugs. Though antipsychotics are often used as first-line medications for Alzheimer's-related agitation, they significantly increase the risk of strokes, heart attacks and death, Lyketsos says.

At the start of the study, patients also underwent tests to define the extent of their agitation, memory and other cognitive skills, and their caregivers' stress levels, a factor strongly linked to the well-being of those with Alzheimer's.

The patients were then separated into two groups. For the next nine weeks, about half took increasing doses of citalopram that peaked at 30 milligrams per day, and the rest took an identical-looking placebo.

At the end of the study period, the same set of tests was given, along with electrocardiograms. The study drug is linked to adverse effects on heart function, including irregular heartbeat, a harbinger of a heart attack.

“Significant relief"

Results showed that patients on the drug had significant relief from their agitation symptoms, Lyketsos says. In one measure of agitation, about 40% of patients who took citalopram had "considerable relief," compared to 26% of patients who took the placebo. The caregivers for these patients reported less stress.

However, patients on the drug were also more likely to have slightly decreased cognitive function. "It was not huge, but measurable," says Lyketsos, director of the Johns Hopkins Memory and Alzheimer's Treatment Center and director of the Department of Psychiatry at Johns Hopkins Bayview Medical Center. "That introduces a tradeoff."

Not without risk

More concerning, he adds, is that patients on citalopram had longer QTc intervals, a measure of abnormal heart function that increases the risk of heart attacks. However, Lyketsos says, antipsychotic medications also used to treat agitation increase heart attack risk as well, perhaps even more substantially.

Lyketsos and his colleagues hope to test if a lower dose of citalopram might be just as effective in treating Alzheimer's-related agitation with less risk for cognition and heart function. In the meantime, he says, the drug offers an alternative to antipsychotics.

"If the agitation is not responding to non-medication treatments and your patient's agitation isn't improving, there are no great options," Lyketsos says. "But here's another medication choice that might be safer than other medications and seems to be just as effective."

Getting a diagnosis of Alzheimer's disease is devastating for both the patient and their loved ones. At present there is no cure and the patient faces a gradual memory loss and, ultimately, death.

After the initial shock a patient may have many questions, not least of which is “how much time do I have?” Doctors currently have no good answer for that, but they might soon. A research team at Columbia University Medical Center (CUMC) has clinically validated a new method they say can predict how long a patient has between diagnosis and full-time care, nursing home residence and death.

The method, which uses data gathered from a single patient visit, is based on a complex model of Alzheimer’s disease progression that the researchers developed by consecutively following two sets of Alzheimer’s patients for 10 years each. Their findings are published in the Journal of Alzheimer's Disease. 

Hard to predict

“Predicting Alzheimer’s progression has been a challenge because the disease varies significantly from one person to another,” said senior author Yaakov Stern, PhD, professor of neuropsychology at CUMC. “Two Alzheimer’s patients may both appear to have mild forms of the disease, yet one may progress rapidly, while the other progresses much more slowly. Our method enables clinicians to predict the disease path with great specificity.”

Stern says the new predictor model – dubbed L-GoM – takes into account the complexity of Alzheimer’s disease. He says patients don’t typically fall neatly into mild, moderate, or severe disease categories and therefore they are uncertain of how much time they have before they begin to feel the degenerative impact of the disease.

“For example, a patient may be able to live independently yet have hallucinations or behavioral outbursts,” said Stern, who also directs the Cognitive Neuroscience Division at CUMC. “Our method is flexible enough to handle missing data. Not all 16 variables are needed for accurate prediction – just as many as are available.”

Too much information?

It may not be the kind of information an Alzheimer's patient wants to have, but it can be vitally important to their caregivers, and to the patient's quality of life.

“In addition to time to nursing home residence or death, our method can be used to predict time to assisted living or other levels of care, such as needing help with eating or dressing, or time to incontinence,” said Ray Razlighi, assistant professor of neurology at CUMC one of the study's authors.

Knowing how long you have before your memory slips away would allow you to be a more active participant in crucial end-of-life decisions and provide a timeline for getting legal and financial affairs in order. For caregivers, knowing what to expect and when might help them get through what will be an extraordinarily difficult time.

Alzhiemer's disease cases are expected to increase rapidly as the large Baby Boom generation enters old age. As many as 5.1 million Americans may currently have Alzheimer's disease, but estimates vary.

The disease

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills, and eventually even the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear after age 60.

According to the National Institutes of Health, memory problems are typically one of the first signs of Alzheimer's disease. Sometimes, other thinking problems, such as trouble finding the right words or poor judgment, are the early warning signs. Other symptoms may include:

• Getting lost
• Trouble handling money and paying bills
• Repeating questions
• Taking longer to complete normal daily tasks
• Poor judgment
• Losing things or misplacing them in odd places
• Mood and personality changes

Near the end, people with severe Alzheimer's cannot communicate and are completely dependent on others for their care. They may be in bed most or all of the time as the body shuts down.

All of this, of course, takes an enormous toll on the caregiver. NIH offers a guide for caregivers that offers advice for coping, starting with the diagnosis. 

Nikolaos Scarmeas, one of the Columbia researchers, says he and his colleagues believe their method of determining the timeline of the Alzheimer's progression will advance efforts to diagnose, treat and manage the effects of this dread disease.

“It may become a valuable tool for both physicians and patients’ families,” he said.

The largest international study ever conducted on Alzheimer's disease has found 11 new regions of the genome involved in the disease, providing new understanding of the underlying molecular processes.

"This study clearly demonstrates that there really is strength in numbers to identify genes that individually have a small effect on risk of Alzheimer's," said Lindsay A. Farrer, PhD, Chief of Biomedical Genetics and professor of medicine, neurology, ophthalmology, genetics & genomics, epidemiology, and biostatistics at Boston University School of Medicine. "But it's not the magnitude of the odds ratio that's really important. Each gene we implicate in the disease process adds new knowledge to our understanding of disease mechanism and provides insight into developing new therapeutic approaches, and ultimately these approaches may be more effective in halting the disease since genes are expressed long before clinical symptoms appear and brain damage occurs," he added.

Since 2009, 10 genes for Alzheimer's disease have been identified. However, much of the individual susceptibility to develop the disease remains unexplained. So in February 2011, the leaders of the four largest international research consortia on the genetics of Alzheimer's joined forces to accelerate the discovery of new genes. Their findings are reported in the current issue of Nature Genetics.

In three years, the researchers identified more genes than had been identified over the previous 20 years. They collected genetic data on 74,076 patients and controls from 15 countries and were able to discover 11 new genes in addition to those already known, and identify 13 other genes, yet to be validated.

These 11 new confirmed genes may open new avenues to understanding the causes of Alzheimer's. For example, one of the most significant findings suggests the involvement of the immune system in the disease. In addition, this same region has also been associated with two other neurodegenerative diseases, one known to have an immune mechanism, multiple sclerosis and another not previously thought to have a major immune component, Parkinson's disease.

The work demonstrates that, given the complexity of such a disease, only a global collaboration of research efforts will quickly find solutions to tackle this major threat, the researchers said.

"Alzheimer's is a complex and devastating disorder, and if we are to reach our goal of finding effective therapies to treat it, then collaboration is key," said Neil Buckholtz, PhD, National Institute on Aging Division of Neuroscience Director. "[The consortium's] sharing of DNA samples, data sets and scientific insights proves that team concept, and NIA is gratified to have provided the infrastructure and support needed to move the team forward."

An analysis of data previously gathered on more than 3,000 older people suggests that the use of certain blood pressure medications may reduce the risk of dementia due to Alzheimer's disease (AD).

The team of Johns Hopkins-led researchers found that people over the age of 75 with normal cognition who used diuretics, angiotensin-1 receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors showed a reduced risk of AD dementia by at least 50%. In addition, diuretics were associated with 50% reduced risk in those in the group with mild cognitive impairment.

However beta blockers and calcium channel blockers did not show a link to reduced risk, the scientists reported.

The report was published in a recent edition of the journal Neurology.

"Identifying new pharmacological treatments to prevent or delay the onset of AD dementia is critical given the dearth of effective interventions to date," says report author, Sevil Yasar, M.D., Ph.D., assistant professor of medicine in the Department of Geriatric Medicine and Gerontology at the Johns Hopkins University School of Medicine. "Our study was able to replicate previous findings, however, we were also able to show that the beneficial effect of these blood pressure medications are maybe in addition to blood pressure control, and could help clinicians in selecting an antihypertensive medication based not only on blood pressure control, but also on additional benefits."

Alzheimer's disease is a rapidly increasing clinical and public health issue in the United States' aging population, and the most common cause of intellectual and social decline.

'Post-hoc' analysis

Yasar and her colleagues conducted a "post-hoc" analysis of information gathered originally in the so-called Ginkgo Evaluation of Memory Study (GEMS) study, a six-year effort to determine if use of the herb ginkgo biloba reduced AD risk.

That study , a double-blind, randomized, controlled clinical trial of 3,069 adults without dementia, aged between 75 and 96 years, began in 2000 and recruited participants from four U.S. cities: Hagerstown, Md.; Pittsburgh, Pa.; Winston-Salem/Greensboro, N.C.; and Sacramento, Calif.

Yasar said that while the GEMS trial showed no benefit of ginkgo biloba in reducing incidence of dementia, information was also available among the study participants related to their use of several classes of antihypertensive drugs.

Extensive studies suggest that high blood pressure is a major risk factor for dementias including AD, and there had been suggestions that drugs used to control blood pressure conferred a protective effect on the brain in addition to controlling blood pressure.

The question, she said, was which ones were associated with reduced AD dementia risk, and which were not.

Yasar and colleagues looked at 2,248 of the GEMS participants. Of them 351 reported use of a diuretic, 140 use of ARBs, 324 use of ACE inhibitors, 333 use of calcium channel blockers and 457 use of beta blockers. The average age of this group was 78.7 years, and 47% were women.

"We were able to confirm previous suggestions of a protective effect of some of these medicines not only in participants with normal cognition, but also in those with mild cognitive impairment," says Yasar. "Additionally, we were also able to assess the possible role of elevated systolic blood pressure in AD dementia by placing those within each medication group in categories above and below systolic blood pressures of 140 mmHg, the standard cut-off reading for a diagnosis of hypertension," she said.

Limitations

Yasar cautioned that the analysis had its limitations, owing mostly to the fact that the data collected by the GEMS trial were not gathered to directly measure the effect of the drugs, and by the fact that it was impossible to tell with certainty how well each group of participants complied with their drug treatments. Nor did the research team have information on subjects' use of drugs prior to the study period.

But, she said, "the consistent pattern we saw of reduced risk of AD dementia associated with these medications warrants further studies, including the use of brain imaging, to better understand the biologic basis of these associations." Such studies, she added, "could lead to identification of new pharmacologic targets for preventive interventions to slow cognitive decline and possibly delay progression of AD dementia."

Researchers at Johns Hopkins say they may have a head start on dealing with Alzheimer's disease.

According to the scientists, by measuring levels of certain proteins in cerebrospinal fluid (CSF), they can predict when people will develop the cognitive impairment associated with Alzheimer's years before the first symptoms of memory loss appear.

Identifying such biomarkers, they say, could provide a long-sought tool to guide earlier use of potential drug treatments to prevent or halt the progression of the ailment while people are still cognitively normal.

Treatment comes too late

Medications designed to stop the brain damage have failed in clinical trials, possibly, many researchers say, because they are given to those who already have symptoms and too much damage to overcome.

"When we see patients with high blood pressure and high cholesterol, we don't say we will wait to treat you until you get congestive heart failure,” says Marilyn Albert, Ph.D., a professor of neurology at the Johns Hopkins University School of Medicine. “Early treatments keep heart disease patients from getting worse, and it's possible the same may be true for those with pre-symptomatic Alzheimer's."

Albert, the primary investigator of the study whose results are published in the Oct. 16 issue of the journal Neurology, adds that “it has been hard to see Alzheimer's disease coming, even though we believe it begins developing in the brain a decade or more before the onset of symptoms."

Testing for proteins

For the new study, the Hopkins team used CSF collected for the Biomarkers for Older Controls at Risk for Dementia (BIOCARD) project between 1995 and 2005, from 265 middle-aged healthy volunteers. Annually during those years and again beginning in 2009, researchers gave the subjects a battery of neuropsychological tests and a physical exam.

They found that particular baseline ratios of two proteins -- phosphorylated tau and beta amyloid found in CSF -- were a harbinger of mild cognitive impairment (often a precursor to Alzheimer's) more than five years before symptom onset. They also found that the rate of change over time in the ratio was also predictive.

The more tau and the less beta amyloid found in the spinal fluid, the more likely the development of symptoms. And, Albert says, the more rapidly the ratio of tau to beta amyloid goes up, the more likely the eventual development of symptoms.

Predictive possibilities

Researchers have known that these proteins were in the spinal fluid of patients with advanced disease. "But we wondered if we could measure something in the cerebral spinal fluid when people are cognitively normal to give us some idea of when they will develop difficulty," Albert says. "The answer is yes."

Alzheimer's disease disrupts critical metabolic processes that keep neurons healthy. These disruptions cause neurons to stop working, lose connections with other nerve cells, and finally die. The brains of people with Alzheimer's have an abundance of two abnormal structures -- amyloid plaques and "tangles" made of tau.

The plaques are sticky accumulations of beta-amyloid that build up outside of the neurons, while the tangles form inside the neurons. When there are too many tangles inside the cells, the cells start to die. In a normal brain, tau helps the skeleton of the nerve cell maintain itself. When too many phosphate groups attach themselves to tau, too much of the protein develops and tangles form.

Albert says researchers believe that the relative amount of beta-amyloid in the spinal fluid decreases as Alzheimer's progresses because it is getting trapped in the plaques and therefore isn't entering the fluid.

Early treatment possible

Though the BIOCARD study has been going on for nearly two decades, this is some of the first predictive data to come out of it, Albert says, owing to the length of time it takes for even high-risk middle-aged people to progress to dementia. Only 53 of the original patients have progressed to mild cognitive impairment or dementia, giving a sample size just large enough to draw some preliminary conclusions. These first symptoms include memory disruptions such as repeating oneself, forgetting appointments, and forgetting what others have said.

Albert cautions that the biomarker ratio at this point is not accurate enough to precisely predict whether a particular individual is progressing to dementia, and further analysis of information about the group over time is needed.

However, she says, if the findings prove valid, they not only could guide the use of early treatments with drugs that become available, but also may also help test new drugs by seeing if they alter the rate at which the proteins change over time.

The last five years have witnessed promising breakthroughs in research into Alzheimer's disease, the fatal condition that robs its victims of their memory as they age. But a lot can happen getting from the scientific experiment level to an approved therapy.

For example, at the beginning of 2013 researchers at the National Institutes of Health (NIH) reported a promising new Alzheimer's treatment. They showed how a molecule called TFP5, when injected into mice with a disease that is the equivalent of human Alzheimer's, symptoms are reversed and memory is restored -- without obvious toxic side effects. 

Could this be a cure for a dread disease? We won't know for a while. The treatment must be subjected to a vigorous clinical trials, which presumably are underway. This is just one of the hopeful developments that have contributed to optimism that Alzheimer's might one day be a non-factor in the aging process.

Most common form of dementia

Alzheimer's is the most common form of dementia, a general term for memory loss and other cognitive abilities serious enough to interfere with daily life. Alzheimer's disease accounts for 50 to 80 percent of dementia cases, according to the Alzheimer's Association. Since getting older is a major risk factor, Alzheimer's is a threat to the large Baby Boom generation.

There are already a number of drugs available to treat the symptoms of Alzheimer's disease and some researchers are working on these existing therapies, to make them more effective. The Salk Institute, the Sanford-Burnham Medical Research Institute and a number of other research entities have defined a key mechanism behind the disease’s progress, giving hope that a newly modified Alzheimer’s drug will be effective.

In 2009 Stephen F. Heinemann, a professor in Salk’s Molecular Neurobiology Laboratory, found that a substance called Alpha7 may help trigger Alzheimer’s disease.

“Previous studies exposed a possible interaction between Alpha-7 nicotinic receptors, labeled ?7Rs, with amyloid beta, the toxic protein found in the disease’s hallmark plaques,” said Gustavo Dziewczapolski, a staff researcher in Heinemann’s lab. “We showed for the first time, in vivo, that the binding of this two proteins, ?7Rs and amyloid beta, provoke detrimental effects in mice similar to the symptoms observed in Alzheimer’s disease.”

Promising results

This week Metabolic Solutions Development Company presented promising results of its Phase 2a study of a new diabetes drug that may prove effective against Alzheimer's. The study found the drug maintained glucose metabolism in key regions of the brain associated with cognitive decline due to Alzheimer's.

Although most research shows Alzheimer's is closely associated with the build-up of harmful plaques in the brain, other inquiries have also shown reducing the role of glucose metabolism in the brain also may play a role.

A key breakthrough? Again, scientists say we may not know for a while, but they applaud the effort.

"We are in urgent need of new approaches in Alzheimer's drug research because there are currently no approved therapies to halt or even slow progression of the disease," said Howard Fillit, MD, Executive Director and Chief Science Officer of the Alzheimer's Drug Discovery Foundation.

Yale discovery

Last week researchers at the Yale School of Medicine reported what they called a breakthrough in understanding and curing Alzheimer's. The scientists have focused on a receptor called metabotropic glutamate receptor 5, or mGluR5, as the missing link in the chain of biological processes that lead to Alzheimer’s disease. 

While all of this is highly encouraging, the proof will be in clinical trials – and time is of the essence. Millions of people are dependent upon the results.

Alzheimer’s disease is estimated to affect more than 26 million people worldwide – more than five million in the U.S. alone. It is only going to get worse as the huge Baby Boomer generation ages. Nearly 106 million people are projected to suffer form the disease by 2050.

It's been suggested before and now British researchers have taken a closer look at evidence that there may be such a thing as being too clean.

Cambridge University researchers say they have found a “very significant” relationship between a nation’s wealth and hygiene and the Alzheimer’s “burden” on its population. High-income, highly industrialized countries with large urban areas and better hygiene exhibit much higher rates of Alzheimer’s.

The theory is that greatly reduced contact with bacteria, viruses and other microorganisms can lead to problems with immune development and an increased risk of dementia.

Using "age-standardized" data -- which predict Alzheimer’s rates if all countries had the same population birth rate, life expectancy and age structure -- the study found strong correlations between national sanitation levels and Alzheimer’s.

Hygiene hypothesis

This latest study adds further weight to the “hygiene hypothesis,” suggesting that sanitized environments may cause the immune system to develop poorly, exposing the brain to the inflammation associated with Alzheimer’s disease.

“The ‘hygiene hypothesis’, which suggests a relationship between cleaner environments and a higher risk of certain allergies and autoimmune diseases, is well- established. We believe we can now add Alzheimer’s to this list of diseases,” said Dr. Molly Fox, lead author of the study and Gates Cambridge Alumna, who conducted the research at Cambridge’s Biological Anthropology division.

The researchers tested whether “pathogen prevalence” can explain the levels of variation in Alzheimer’s rates across 192 countries.

After adjusting for differences in population age structures, the study found that countries with higher levels of sanitation had higher rates of Alzheimer’s. For example, countries where all people have access to clean drinking water, such as the UK and France, have 9% higher Alzheimer’s rates than countries where less than half have access, such as Kenya and Cambodia.

Countries that have much lower rates of infectious disease, such as Switzerland and Iceland, have 12% higher rates of Alzheimer’s compared with countries with high rates of infectious disease, such as China and Ghana.

Previous research has shown that in the developed world, dementia rates doubled every 5.8 years compared with 6.7 years in low income, developing countries; and that Alzheimer’s prevalence in Latin America, China and India are all lower than in Europe, and, within those regions, lower in rural compared with urban settings -- supporting the new study’s findings.

The results of the study appear in journal Evolution, Medicine and Public Health.

Younger people likely don't spend a lot of time thinking about Alzheimer's Disease, but maybe they should -- especially women who are new mothers or are about to become mothers.

A new study suggests that mothers who breastfeed run a lower risk of developing Alzheimer's and that longer periods of breastfeeding further reduces the risk

The report, published in the Journal of Alzheimer's Disease, suggests the link may have to do with certain biological effects of breastfeeding. For example, breastfeeding restores insulin tolerance which is significantly reduced during pregnancy, and Alzheimer's is characterized by insulin resistance in the brain.

Strong evidence

Although researchers used data gathered from a very small group of just 81 British women, they observed a highly significant and consistent correlation between breastfeeding and Alzheimer's risk. They argue that this was so strong that any potential sampling error was unlikely.

At the same time, however, the connection was much less pronounced in women who already had a history of dementia in their family. The research team hopes the study -- which was intended merely as a pilot -- will stimulate further research into the relationship between female reproductive history and disease risk.

The findings may point towards new directions for fighting the global Alzheimer's epidemic -- especially in developing countries where cheap, preventative measures are desperately needed.

Understanding the disease

More broadly, the study opens up new lines of inquiry into understanding what makes someone susceptible to Alzheimer's in the first place. It may also act as an incentive for women to breastfeed, rather than bottle-feed -- something already known to have wider health benefits for both mother and child.

"Alzheimer's is the world's most common cognitive disorder and it already affects 35.6 million people,” said Dr. Molly Fox of the Department of Biological Anthropology at the University of Cambridge, who led the study. “In the future, we expect it to spread most in low and middle-income countries. So it is vital that we develop low-cost, large-scale strategies to protect people against this devastating disease."

Previous studies have already established that breastfeeding can reduce a mother's risk of certain other diseases, and research has also shown that there may be a link between breastfeeding and a woman's general cognitive decline later in life. Until now, however, little has been done to examine the impact of breastfeeding duration on Alzheimer's risk.

The study

Fox and her colleagues interviewed 81 British women aged between 70 and 100, including both women with and without Alzheimer's. In addition, the team also spoke to relatives, spouses and caregivers.

Through these interviews, the researchers collected information about the women's reproductive history, their breastfeeding history and their dementia status. They also gathered information about other factors that might account for their dementia -- for example a past stroke or brain tumor.

Dementia status itself was measured using a standard rating scale called the Clinical Dementia Rating (CDR). The researchers also developed a method for estimating the age of Alzheimer's sufferers at the onset of their disease, using the CDR as a basis and taking into account their age and existing, known patterns of Alzheimer's progression. All of this information was then compared with the participants' breastfeeding history.

Despite the small number of participants, the study revealed a number of clear links between breastfeeding and Alzheimer's. These were not affected when the researchers took into account other potential variables such as age, education history, the age when the woman first gave birth, her age at menopause,or her smoking and drinking history.

Main trends found

The researchers observed three main trends:

• Women who breastfed exhibited a reduced Alzheimer's Disease risk compared with women who did not.
• Longer breastfeeding history was significantly associated with a lower Alzheimer's Risk.
• Women who had a higher ratio of total months pregnant during their life to total months breastfeeding had a higher Alzheimer's risk.

The trends were, however, far less pronounced for women who had a parent or sibling with dementia. In these cases, the impact of breastfeeding on Alzheimer's risk appeared to be significantly lower than for women whose families had no history of dementia.

Explaining the connection

The study argues that there may be a number of biological reasons for the connection between Alzheimer's and breastfeeding, all of which require further investigation.

One theory is that breastfeeding deprives the body of the hormone progesterone, compensating for high levels of progesterone which are produced during pregnancy. Progesterone is known to desensitize the brain's estrogen receptors, and estrogen may play a role in protecting the brain against Alzheimer's.

Another possibility is that breastfeeding increases a woman's glucose tolerance by restoring her insulin sensitivity after pregnancy. Pregnancy itself induces a natural state of insulin resistance. This is significant because Alzheimer's is characterized by a resistance to insulin in the brain (and therefore glucose intolerance) to the extent that it is even sometimes referred to as "Type 3 diabetes".

"Women who spent more time pregnant without a compensatory phase of breastfeeding therefore may have more impaired glucose tolerance, which is consistent with our observation that those women have an increased risk of Alzheimer's disease," Fox concluded.

Pharmaceutical companies invest billions in research on drugs and treatment for Alzheimer's disease, but a British study suggests inexpensive vitamins may be just as helpful.

A study at the University of Oxford found that B vitamins, in particular, can help reduce brain shrinkage for older people with dementia and other memory ailments. In a 2010 clinical trial, patients taking vitamin B had significantly slower total brain shrinkage.

It's no cure, of course, but the scientists suggest it's a cheap way to slow the onset of the fatal disease that robs its victims of memory function. Some physicians have been recommending vitamin B for older patients for years.

Improves memory

“Vitamin B-12 helps maintain healthy nerve cells and red blood cells,” according to Glen Smith, PhD., of the Mayo Clinic. “A vitamin B-12 deficiency — most common in older adults and vegetarians — can cause various signs and symptoms, including memory loss. In such cases, vitamin B-12 supplements can help improve memory.”

To date there is no evidence to suggest that vitamin B-12 supplements enhance memory if you already have Alzheimer's disease. Vitamin B-12 is found naturally in foods that come from animals, including fish, meat and poultry. In addition, a lot of popular breakfast cereals are fortified with vitamin B-12.

If vitamin B does, in fact, prove effective at delaying the onset of Alzheimer's, it could prove to be an inexpensive way to postpone what is expected to be a wave of new cases as the large baby boom generation moves into old age. Meanwhile, research on cure and prevention continues.

Cancer drug

Researchers at the University of Pittsburgh Graduate School of Public Health say a drug used mostly against cancer has been found to reverse memory deficits in a study using mice.

The researchers studied results of tests on the drug bexarotene, which is a Food and Drug Administration (FDA)-approved drug for use in treating cutaneous T cell lymphoma. The Pitt Public Health researchers were able to verify that the drug significantly improves memory deficits in mice expressing gene mutations linked to human Alzheimer's disease. However, they say they could not confirm the effect on amyloid plaques, which are believed to be a leading Alzheimer's trigger.

"We believe these findings make a solid case for continued exploration of bexarotene as a therapeutic treatment for Alzheimer's disease," said senior author Dr. Rada Koldamova.

The Pitt study is just the latest in a number of recent research efforts that have reported promising breakthroughs in either treating or preventing the disease, but that have yet to bear any fruit.

Recent research

A 2006 study in the American Journal of Medicine suggested three or more servings of fruit juice per week netted a 76% reduction in Alzheimer's risk.

In 2008 British researchers said they had developed a drug that, taken daily in pill form, stops Alzheimer's disease in its tracks. The drug is known as Rember, and scientists reported it appeared to be twice as effective as current Alzheimer's treatments, reducing the effects of the memory-robbing disease by as much as 81 percent.

In 2012 researchers at the Mayo Clinic in Florida reported discovery of an enzyme that could represent a powerful new tool for combating Alzheimer's disease. The enzyme -- known as BACE2 -- destroyed beta-amyloid, a toxic protein fragment that litters the brains of patients who have the disease, in clinical trials.

Meanwhile, the threat from Alzheimer's disease seems to grow each year as the population ages. According to the Alzheimer's Association Alzheimer's disease is the sixth leading cause of death in the United States and more than five million Americans are currently living with the disease.

It says that in 2012, 15.4 million caregivers provided more than 17.5 billion hours of unpaid care valued at $216 billion.  

You may not remember why you started taking ginkgo biloba but it was probably because it's said to improve your memory. That's fine, but a new government study finds it may also be carcinogenic.

Researchers at the National Toxicology Program (NTP) fed the stuff to rats and mice over a two-year period and found that the rodents were more likely to develop thyroid and liver tumors than those who had managed to steer clear of the stuff.

In a shorter, three-month test, rats and mice who were given ginkgo showed early signs of tumor growth.

According to the 2007 National Health Interview Survey, ginkgo is one of the top 10 natural products used by Americans, so it's important to learn its relative safety and effectiveness. As for how -- and whether -- the results have implications for humans, the researchers say, as they so often do, that more research is needed.

But that doesn't stop pill pushers who sell the supplement from making  promises that, in many cases, aren't backed by solid research.

"Scientific research documents the ability of ginkgo to maintain peripheral circulation to the arms, legs and brain. In addition, ginkgo helps improve memory, especially occasional mild memory problems associated with aging," says Walgreens.com, adding that its claims "have not been evaluated by the Food and Drug Administration" and that, "This product is not intended to diagnose, treat, cure or prevent any disease."

What good is it?

When making a decision about swallowing supplements, it's a good idea to look not just at the possible dangers but also at the documented benefits. In the case of ginkgo, guess what? There are none.

A 2008 study published in the Journal of the American Medical Association found ginkgo "ineffective in reducing the development of dementia and Alzheimer’s disease in older people."

Known as the Ginkgo Evaluation of Memory (GEM) study, the research was carried out at four clinical sites over the course of 8 years. GEM is the largest clinical trial ever to evaluate ginkgo’s effect on the occurrence of dementia.

“We have made enormous progress in understanding the basic mechanisms involved in Alzheimer’s disease, and we continue to pursue a vigorous program to translate what we know into the development and testing of new potential therapies for this devastating disease,” said Richard Hodes, M.D., director of the National Institute on Aging, part of the National Institues of Health. “However, it is disappointing that the dietary supplement tested in this study had no effect in preventing Alzheimer’s disease.”

GEM enrolled 3,069 participants age 75 or older with normal cognition or mild cognitive impairment. Participants were randomly assigned to receive twice-daily doses of either 120 milligrams of ginkgo extract or an identical-appearing placebo. 

Impressive tumors

Stack that up against the findings involving mice and rats.

“The tumors found in mice were pretty impressive,” Dr. Cynthia Rider, NTP’s study scientist for ginkgo, told Food Safety News. “They were among the highest in NTP studies for one of the tumors that doesn’t occur simultaneously all the time in mice.”

You can read the entire study abstract here but perhaps the most important thing to remember is that ginko just could be one of those things that does more harm than good.  

It's a pretty well-established fact that stress can cause numerous health  problems. But now there may be a new concern.

Researchers at Umea University in Sweden say psychological stress during middle age could cause one to develop Alzheimer’s disease years later.

The scientists looked at the stress hormones in the brains of mice and found those with more stress had less memory. In addition, the brains of the mice with more stress had larger amounts of beta amyloid, a protein that’s associated with Alzheimer’s disease.  

In a 2007 study, researchers discovered the connection between beta amyloids and Alzheimer’s disease.

“Beta amyloid is associated with brain dysfunction — even in apparently normal elderly individuals — providing further evidence that it is likely related to the fundamental cause of Alzheimer’s disease,” explained Christopher Rowe, director of the nuclear medicine department and Centre for PET, at Austin Hospital in Australia.

In addition, the researchers involved in the 2007 study said that beta amyloid led to common Alzheimer’s symptoms like memory loss and brain synapses.

More study needed

Dr. Simon Ridley, director of research at Alzheimer’s Research UK, said additional studies involving humans is needed,

“Some research has already highlighted a possible link between chronic stress, cognitive decline and the development of Alzheimer’s, and further study in people is needed to fully investigate these links,” he said. “If we can better understand the risk factors for Alzheimer’s we can also empower people to make lifestyle changes to reduce their risk.”

Additionally, researchers said people who use their brain in high capacity throughout life, like learning new languages or being in a job that requires a lot of critical thinking, have less risk of developing Alzheimer’s later in life.

Exercise may help

In a separate study at the University of Helsinki, Finland, researchers found that intensive exercise at home has the ability to slow down some of the symptoms associated with Alzheimer’s.

Researchers gathered 210 Alzheimer patients who lived at home with their spouses and split the groups into three.

One trial group had four-hour group sessions with one hour of home-based exercise; one group only had one hour of exercise and the other group received traditional care.

Although all groups in the study showed signs of deterioration as time went on, the group that went through four-hour sessions and one hour of training had the least amount.

Furthermore, the researchers made a connection between Alzheimer’s patients who exercised in their home and the possibility of keeping health and social services costs down.

The group that underwent four-hour training sessions and one hour of exercise had a total health and social service cost of $22,066. The second group, undergoing only one hour of exercise, ran a cost of $25,112 and the group that received traditional care had a health and social service cost of $34,121.

The lower costs along with the ability to possibly slow down physical deterioration in Alzheimer’s patients, shows how beneficial exercising at home can be, say researchers.

“In conclusion, this study demonstrates that exercise administered at the patient’s home may attenuate the deleterious effects of AD on physical functioning,” the researchers wrote.

According to the Alzheimer’s Association, Alzheimer’s disease is the sixth leading cause of death in the United States and over 5 million Americans currently live with the disease. In addition, one in three seniors who have Alzheimer’s or other dementia passes away.

Rats engineered to have the mutant genes that are known to play a role in the rare, early-onset form of Alzheimer’s disease are being used in the effort to determine the cause of the disabling disease.

A study, published in the Journal of Neuroscience, says rodents that have the full array of brain changes associated with Alzheimer’s disease supports the idea that increases in a molecule called beta-amyloid in the brain causes the disease.

“We believe the rats will be an excellent, stringent pre-clinical model for testing experimental Alzheimer’s disease therapeutics,” said Terrence Town, Ph.D., the study’s senior author and a professor in the Department of Physiology & Biophysics in the Zilkha Neurogenetic Institute at the University of Southern California Keck School of Medicine, Los Angeles.

An age-related brain disorder that gradually destroys a person’s memory, thinking, and the ability to carry out even the simplest tasks, Alzheimer's affects at least 5.1 million Americans and is the most common form of dementia in the United States.

A new breed

Researchers often use rodents to study diseases. However, previous studies on transgenic mice and rats that have the gene mutations only partially reproduce the problems caused by Alzheimer’s. The animals have memory problems and many plaques but none of the other hallmarks, especially neurofibrillary tangles and neuron loss.

To address this issue, Dr. Town and his colleagues decided to work with a certain strain of rats.“We focused on Fischer 344 rats,” he said, “because their brains develop many of the age-related features seen in humans.”

“This new rat model more closely represents the brain changes that take place in humans with Alzheimer’s, including tau pathology and extensive neuronal cell death,” said Roderick Corriveau, Ph.D., a program director at the National Institute of Neurological Disorders and Stroke. The model, he said, “will help advance our understanding of the various disease pathways involved in Alzheimer’s onset and progression and assist us in testing promising interventions.”

We're living longer -- no doubt about that. But it comes with a cost, especially when you consider mental health.

Researchers say the costs of caring for people with dementia in the United States ran as high as $215 billion in 2010 and -- with the increase in the elderly population in the years ahead -- is likely to rise even more.

In comparison, in the same year it cost $102 billion to care for those with heart disease$77 billion for cancer care.

You can find more information at the website of the National Institutes of Health.

An enzyme that could represent a powerful new tool for combating Alzheimer's disease has been discovered by researchers at Mayo Clinic in Florida. The enzyme -- known as BACE2 -- destroys beta-amyloid, a toxic protein fragment that litters the brains of patients who have the disease. 

The findings were published online in the science journal Molecular Neurodegeneration. 

Alzheimer's disease is the most common memory disorder. It affects more that 5.5 million people in the United States. Despite the disorder's enormous financial and personal toll, effective treatments have not yet been found. 

More effective than other enzymes 

The Mayo research team, led by Malcolm A. Leissring, Ph.D., a neuroscientist at Mayo Clinic in Florida, made the discovery by testing hundreds of enzymes for the ability to lower beta-amyloid levels. BACE2 was found to lower beta-amyloid more effectively than all other enzymes tested. The discovery is interesting because BACE2 is closely related to another enzyme, known as BACE1, involved in producing beta-amyloid. 

"Despite their close similarity, the two enzymes have completely opposite effects on beta-amyloid -- BACE1 giveth, while BACE2 taketh away," Dr. Leissring says. 

Beta-amyloid is a fragment of a larger protein, known as APP, and is produced by enzymes that cut APP at two places. BACE1 is the enzyme responsible for making the first cut that generates beta-amyloid. 

The research showed that BACE2 cuts beta-amyloid into smaller pieces, thereby destroying it, instead. Although other enzymes are known to break down beta-amyloid, BACE2 is particularly efficient at this function, the study found. 

Previous work had shown that BACE2 can also lower beta-amyloid levels by a second mechanism: by cutting APP at a different spot from BACE1. BACE2 cuts in the middle of the beta-amyloid portion, which prevents beta-amyloid production. 

Attractive treatment candidate 

"The fact that BACE2 can lower beta-amyloid by two distinct mechanisms makes this enzyme an especially attractive candidate for gene therapy to treat Alzheimer's disease," says first author Samer Abdul-Hay, Ph.D., a neuroscientist at Mayo Clinic in Florida. 

The discovery suggests that impairments in BACE2 might increase the risk of Alzheimer's disease. This is important because certain drugs in clinical use -- for example, antiviral drugs used to treat human immunodeficiency virus (HIV) -- work by inhibiting enzymes similar to BACE2. 

Although BACE2 can lower beta-amyloid by two distinct mechanisms, only the newly discovered mechanism -- beta-amyloid destruction -- is likely relevant to the disease, the researchers note. This is because the second mechanism, which involves BACE2 cutting APP, does not occur in the brain.

The researchers have obtained a grant from the National Institutes of Health to study whether blocking beta-amyloid destruction by BACE2 can increase the risk for Alzheimer's disease in a mouse model of the disease.

A repression of gene activity in the brain appears to be an early event affecting people with Alzheimer's disease, researchers funded by the National Institutes of Health have found. In mouse models of Alzheimer's disease, this epigenetic blockade and its effects on memory were treatable.

"These findings provide a glimpse of the brain shutting down the ability to form new memories gene by gene in Alzheimer's disease, and offer hope that we may be able to counteract this process," said Roderick Corriveau, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research.

Dr. Li-Huei Tsai and her team at the Massachusetts Institute of Technology and the Howard Hughes Medical Institute found that a protein called histone deacetylase 2 (HDAC2) accumulates in the brain early in the course of Alzheimer's disease in mouse models and in people with the disease.

HDAC2 is known to tighten up spools of DNA, effectively locking down the genes within and reducing their activity, or expression.

In the mice, the increase in HDAC2 appears to produce a blockade of genes involved in learning and memory. Preventing the build-up of HDAC2 protected the mice from memory loss.

Dr. Tsai and her team examined two mouse models of Alzheimer's around the time that the mice begin to show signs of brain cell degeneration. They found that the mice had higher levels of HDAC2, but not other related HDAC proteins, specifically in the parts of the brain involved in learning and memory. This increase in HDAC2 was associated with a decrease in the expression of neuronal genes that HDAC2 is known to regulate.

Gene therapy

Dr. Tsai and her team also examined HDAC2 levels in autopsied brain tissue from 19 people with Alzheimer’s at different stages of the disease, and from seven unaffected individuals. Even in its earliest stages, the disease was associated with higher HDAC2 levels in the learning and memory regions of the brain.

"We think that the blockade of gene expression plays a very important role in the cognitive decline associated with Alzheimer's disease," said Dr. Tsai. "The good news is that the blockade is potentially reversible."

Alzheimer's disease is the most common cause of dementia in older adults, and affects as many as 5.1 million Americans. In the most common type of Alzheimer's disease, symptoms usually appear after age 65. A hallmark of the disease is the accumulation of a toxic protein fragment called beta-amyloid in brain cells, which is widely believed to be the initial trigger for neurodegeneration.

Dr. Tsai theorizes that HDAC2 is brought into play by beta-amyloid. Indeed, she and her team found that exposing mouse neurons to beta-amyloid caused them to produce more HDAC2.

When it comes to Alzheimer's disease, researchers say size matters. Brain size, that is.

The study suggests that, in people who don’t currently have memory problems, those with smaller regions of the brain’s cortex may be more likely to develop symptoms consistent with very early Alzheimer’s disease.

“The ability to identify people who are not showing memory problems and other symptoms but may be at a higher risk for cognitive decline is a very important step toward developing new ways for doctors to detect Alzheimer’s disease,” said Susan Resnick, PhD, with the National Institute on Aging in Baltimore, who wrote an accompanying editorial.

For the study, researchers used brain scans to measure the thickness of regions of the brain’s cortex in 159 people free of dementia with an average age of 76. The brain regions were chosen based on prior studies showing that they shrink in patients with Alzheimer’s dementia.

Of the 159 people, 19 were classified as at high risk for having early Alzheimer’s disease due to smaller size of particular regions known to be vulnerable to Alzheimer’s in the brain’s cortex, 116 were classified as average risk and 24 as low risk. At the beginning of the study and over the next three years, participants were also given tests that measured memory, problem solving and ability to plan and pay attention.

The study found that 21 percent of those at high risk experienced cognitive decline during three years of follow-up after the MRI scan, compared to seven percent of those at average risk and none of those at low risk.

More research needed

“Further research is needed on how using MRI scans to measure the size of different brain regions in combination with other tests may help identify people at the greatest risk of developing early Alzheimer’s as early as possible,” said study author Bradford Dickerson, MD, of Massachusetts General Hospital in Boston and a member of the American Academy of Neurology.

The study also found 60 percent of the group considered most at risk for early Alzheimer’s disease had abnormal levels of proteins associated with the disease in cerebrospinal fluid, which is another marker for the disease, compared to 36 percent of those at average risk and 19 percent of those at low risk.

A parent or loved one who has begun to have problems with balance could be experiencing early indicators of Alzheimer's disease, according to researchers at Washington University School of Medicine in Saint Louis.

The researchers reported their findings this week at the Alzheimer’s Association International Conference on Alzheimer’s Disease in Paris.

They found that study participants with brain changes suggestive of early Alzheimer’s disease were more likely to fall than those whose brains did not show the same changes. Until now, falls had only been associated with Alzheimer’s in the late stages of dementia.

No obvious signs of Alzheimer's

“If you meet these people on the street, they appear healthy and have no obvious cognitive problems,” said lead author Susan Stark, PhD, assistant professor of occupational therapy and neurology. “But they have changes in their brain that look similar to Alzheimer’s disease, and they have twice the typical annual rate of falls for their age group.”

About one in three adults age 65 or older typically fall each year. But in the 18 participants with high amyloid levels in the brain, a hallmark of Alzheimer's disease, two-thirds fell within the first eight months of the study. High levels of amyloid in the brain were the best predictor of an increased risk of falls.

“Falls are a serious health concern for older adults,” Stark said. “Our study points to the notion that we may need to consider preclinical Alzheimer’s disease as a potential cause.”

Inherited Alzheimer's

In an unrelated study at the university, researchers found that inherited forms of Alzheimer's may be detectable as many as 20 years before memory problems surface. The discovery, they say, may lead to much earlier diagnosis, which could slow the impact of the progressive disease.

“We want to prevent damage and loss of brain cells by intervening early in the disease process — even before outward symptoms are evident, because by then it may be too late,” said Alzheimer’s researcher and physician Randall Bateman, MD, of Washington University School of Medicine in St. Louis and an associate director of the Dominantly Inherited Alzheimer’s Network (DIAN), an international study of inherited forms of Alzheimer’s.

Scientists may be a step closer to unraveling the mysteries of Alzheimer's disease and finding a cure for the dreaded affliction that robs the aging of their memory.

Researchers say they have identified four more genes that may serve as triggers for the onset of the disease. With this information, they say, they may be able to devise a drug, or therapeutic lifestyle, that can prevent more than have the cases.

Four of the new genes are linked to late-onset Alzheimer's disease. Each of these genes adds to the risk of developing this most common form of the disease, and together they offer a portal into the causes of Alzheimer's.

New pathways

"A significant aspect of our research is that these genes clarify three new pathways," said Richard Mayeux, one of the lead scientists in the study and Chairman of the Department of Neurology of Columbia University Medical Center.

The genes are related to the accumulation of amyloid in the brain. These new genes are involved in inflammatory processes, lipid metabolism, and the movement of molecules within cells.

"Therefore, we may now have four pathways that are critically related to the disease and that could really make a difference in how we study and potentially prevent and treat it," ssaid Mayeux.

Intriguing results

The study also revealed other intriguing results.  Dr. Michael Boehnke, a professor at the University of Michigan and an outside advisor to the study, says researchers found that injuries that cause an inflammation of the brain --  such as strokes and head injuries  -- increases the risk of Alzheimer's.

He also says that the study found that some of the newly discovered genes appear to be affected by cholesterol, leading researchers to conclude that people with high levels of cholesterol are more at risk for Alzheimer's disease.

The study is one of the largest of its kind. It was led by the University of Pennsylvania School of Medicine, the University of Miami, Boston University School of Medicine and Columbia University. It analyzed more than 11,000 people with Alzheimer's and a nearly equal number of elderly people with no symptoms of dementia. In all, it studied about 54,000 individuals.

"This is the culmination of years of work on Alzheimer's disease by a large number of scientists, yet it is just the beginning in defining how genes influence memory and intellectual function as we age. We're all tremendously excited by our progress so far, but much remains to be done, both in understanding the genetics and in defining how these genes influence the disease process," said Gerald D. Schellenberg, a University of Pennsylvania researcher.

Objectives

The research had two main objectives. First, identification of new Alzheimer's disease genes will provide major clues as to its underlying cause. Scientists say the knowledge gained from this study will lead to development of more effective drugs.

Second, the gene discovery will help physicians predict who is at greatest risk of developing Alzheimer's disease. This, researchers say, will be important as preventive measures become available. Identification of these risk genes will also help researchers to determine the disease-initiating steps that begin in the brain long before any symptoms of memory loss or intellectual decline are apparent.

Eventually, it is hoped that researchers will be able to describe the events that lead to the destruction of large parts of the brain and, ultimately, complete loss of cognitive abilities.

Research has suggested a genetic link to Alzheimer's disease. If one of your parents has it, the risk that you will one day get it increases.

Now, results from a new study finds that if it is your mother who has the cognitive illness, the odds against your are even greater. The study is published in the March 1, 2011, print issue of Neurology, the medical journal of the American Academy of Neurology.

"It is estimated that people who have first-degree relatives with Alzheimer's disease are four to 10 times more likely to develop the disease themselves compared to people with no family history," said study author Robyn Honea, DPhil, of the University of Kansas School of Medicine in Kansas City.

For the study, an equal number of participants had a father with Alzheimers and an equal number had a mother with the illness. The groups were given brain scans and cognitive tests throughout the study.

Twice the gray matter shrinkage

The researchers found that people with a mother who had Alzheimer's disease had twice as much gray matter shrinkage as the groups who had a father or no parent with Alzheimer's disease.

In addition, those who had a mother with Alzheimer's disease had about one and a half times more whole brain shrinkage per year compared to those who had a father with the disease. Shrinking of the brain, or brain atrophy, occurs in Alzheimer's disease.

"Using 3-D mapping methods, we were able to look at the different regions of the brain affected in people with maternal or paternal ties to Alzheimer's disease," said Honea. "In people with a maternal family history of the disease, we found differences in the break-down processes in specific areas of the brain that are also affected by Alzheimer's disease, leading to shrinkage. Understanding how the disease may be inherited could lead to better prevention and treatment strategies."

Growing threat

Alzheimer's continues to be the focus of intense medical research as millions of Baby Boomers enter the age in which they are at risk. A 2010 report by the Alzheimer's Association projects that as many as 10 million baby boomers in the U.S. will eventually develop Alzheimer's, a degenerative and always fatal disease.

Today, as many as 5.2 million Americans are living with Alzheimer's disease, which includes between 200,000-500,000 people under age 65 with young-onset Alzheimer's disease or other dementias. Medical researchers predict by 2010, there will be almost a half million new cases of Alzheimer's disease each year; and by 2050, there will be almost a million new cases each year.

Eventually, the report says, the disease will strike one out of every eight Boomers.

Many adult children have struggled with the thorny issue of taking the car keys from an aging parent or grandparent. But how do you know when to take away the checkbook?

When an older person begins to show confusion in managing their financial affairs, it can be a warning that the person is suffering from Alzheimer's disease and its pre-cursor, mild cognitive impairment (MCI).

Physicians need to help patients and families recognize when an older patient is losing the ability to manage their own financial affairs, say researchers at the University of Alabama at Birmingham and the University of California at San Francisco. Their study appears in the  Journal of the American Medical Association.

Financial abilities decline

"Financial capacity is essential for an individual to function independently in our society," said study co-author Daniel Marson, J.D., Ph.D., professor of neurology and director of the UAB Alzheimer's Disease Center. "Diagnosis of cognitive impairment generally, and MCI and Alzheimer's disease specifically, should signal likely financial impairment and prompt physicians to encourage patients and families to seek financial and legal advance planning."

The commentary from Marson and colleagues is part of JAMA's "Care of the Aging Patient: From Evidence to Action" series that provides evidence-based clinical guidance to physicians. Patients with MCI typically still are functioning in the community with focal memory or other cognitive impairments but are beginning to show initial signs of functional decline.

New tool

In 2009, Marson and his group published a major paper on declining financial capacity in MCI and progression to Alzheimer's, which involved a tool developed at UAB called the Financial Capacity Instrument. The FCI measures capacity across 20 tasks, including understanding a bank statement, balancing a checkbook, paying bills, preparing bills for mailing and counting coins and currency.

"Declining financial capacity is a good barometer for progression of both MCI and Alzheimer's disease," said Marson, "Our previous research has shown that a decline in checkbook-management skills can be a harbinger of a patient's progression from MCI to early Alzheimer's dementia. Emerging impairments in financial skills and judgment often are the first functional changes demonstrated by patients with incipient dementia."

Scientists are seeking ways to detect the earliest stages of Alzheimer's disease, since harmful changes may be taking place in the brain years before symptoms appear.

Now, researchers report that a blood test detecting a specific protein in blood samples from cognitively normal older people may reflect the levels of beta-amyloid protein in the brain-- a hallmark of the disease.

Findings of the study, supported in part by the National Institutes of Health (NIH), may eventually lead to a blood test that helps predict risk for Alzheimer's disease and who may be a good candidate for participating in clinical trials.

"Recent advances in imaging and biomarkers that help track the onset and progression of Alzheimer's disease show promise for early detection of the disease process, and for tracking the effectiveness of early interventions," said National Institute on Aging (NIA) Director Richard J. Hodes, M.D. "This is critically important in streamlining and conducting trials more efficiently so that we can find out about possible therapies that much sooner."

Protein study

Using proteomics technology, a method of studying hundreds of proteins from a small blood sample, the researchers analyzed blood samples of 57 older and symptom-free volunteers to determine whether specific proteins were associated with amyloid burden in the brain.

They measured brain amyloid using PET (positron emission tomography) scans with Pittsburgh Compound B, a tracer that binds to amyloid plaques. The volunteers are participating in the NIA's Baltimore Longitudinal Study of Aging (BLSA), America's longest-running scientific study of human aging.

The researchers found the amount of a specific protein called apolipoprotein E, or ApoE, in the blood samples was strongly associated with the level of beta amyloid in the brain. Those with high blood levels of the protein had significantly greater deposits of amyloid in the medial temporal lobe, the region of the brain important to memory function.

'Intriguing' results

"These results are especially intriguing as this protein is made by the APOE gene, the most robust genetic risk factor for late-onset Alzheimer's," said Madhav Thambisetty, M.D., Ph.D., of the Intramural Research Program atNIA, the lead author on the study. Late-onset Alzheimer's is the most common form of the disease and occurs around age 65 or later.

He now plans to test these findings in serial blood samples collected every year in BLSA volunteers to determine how changing blood levels of ApoE protein may relate to pathological changes in the brain over time.

"If the results are equally positive, we may be able to develop a blood test that provides a less invasive, inexpensive method that helps to detect the early pathological changes of Alzheimer's disease," he said.

The study appears in the Dec. 20, 2010, issue of the Journal of Alzheimer's Disease.

Worried you or a loved one might be showing signs of Alzheimer's disease? Researchers say a new test can let you know for sure in about 30 seconds time.

A new study, led by Professor David Bunce, while at the Center for Mental Health Research at The Australian National University, has revealed that some apparently healthy adults aged between 44 and 48 years have tiny, white matter lesions in areas of their brains similar to those found in persons with Alzheimer's later in life.

These lesions can potentially be predicted via a 30-second test that measures a patient's response time. With further research, the test could become commonplace in GPs' surgeries within two years.

The research also suggests that the neurological decline thought to lead to the development of Alzheimer's disease may begin much earlier in people's lives than was originally thought.

Signs can be present in people in their 40s

"Although we cannot be certain that these middle-aged people will go on to get dementia, the results are important," Bunce said. "First, the study is one of the first to show that lesions in areas of the brain that deteriorate in dementia are present in some adults aged in their 40s. Second, although the presence of the lesions was confirmed through MRI scans, we were able to predict those persons who had them through very simple tests."

If the findings are repeated in laboratories elsewhere, Bunce says the study lays open possibilities for screening, early detection and intervention in healthcare settings.

"The earlier we can intervene with people vulnerable to eventual dementia, the greater the chances of preventing or delaying the disease onset,” he said.

The researchers' paper, 'Cognitive Deficits are associated with Frontal and Temporal Lobe White Matter Lesions in Middle-Aged Adults Living in the Community' is published in the open-access journalPublic Library of Science-One.

Looming problem

With the huge baby boom generation headed told old age, health officials are worried that Alzheimer's could reach epidemic proportions in the years ahead. For that reason researchers have refocused their efforts, not just on early detection but an effective treatment.

As of now, there is no cure for Alzheimer's disease, though some recent research has shown promise. In July, Researchers at the Institute of Psychiatry at King's College London reported that a simple blood test could soon give Alzheimer's patients ten years advance warning that they will get the disease. The breakthrough came after researchers found high levels of a protein can be an early sign of the condition.

Alzheimer's is a brain disease that causes problems with memory, thinking and behavior.Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Although current Alzheimer's treatments cannot stop the disease from progressing, they can temporarily slow the symptoms and improve the quality of life for those with the disease and their caregivers.

Researchers at the Institute of Psychiatry at King's College London say a simple blood test could soon give Alzheimer's patients ten years advance warning that they will get the disease.

The breakthrough came after researchers found high levels of a protein can be an early sign of the condition.

The study, published in the Archives of General Psychiatry, has found that clusterin levels in blood could be an early biomarker of AD many years before symptoms appear. The international team of scientists also found that higher levels of clusterin were related to more severe and rapid memory loss and greater brain shrinkage.

It is these findings, they say, that could lead to development of a blood test to help identify who would benefit from early treatment of AD and also whether treatments were working to delay or prevent brain damage.

Researchers have been focusing on developing an inexpensive blood test that will accurately reflect the damage detected by brain scans in patients in the early stages of AD, such as shrinkage ("atrophy") in certain regions and abnormal accumulations of a protein called beta amyloid.

In this study, researchers used a novel strategy combining brain scans with proteomics, a method that can detect hundreds of proteins in a single blood sample. They compared blood samples and brain scans of 300 research participants with AD, mild cognitive impairment or normal cognition.

They found that a single protein -- clusterin -- was related to brain shrinkage, severity of memory problems and a risk of faster memory loss. Using the same method in blood samples from volunteers in a continuing study in the United States, they showed that increased amounts of clusterin -- measured a decade earlier to the brain scans -- were linked to higher levels of beta amyloid in the brain.

Finally, in mouse models of AD, researchers discovered increased levels of clusterin in the blood as the mice aged. Under the microscope, they also observed clusterin to be surrounding the amyloid plaques.

They concluded this provides further evidence that clusterin is critically important in Alzheimer's where it probably works to help protect the brain from amyloid protein. This finding from proteomics complements the discovery reported last year by an international team including the KCL group that showed the clusterin gene increased risk of AD -- a finding noted by Time magazine as one of the top ten medical discoveries of 2009.

Easy test

"A primary goal in Alzheimer's research is to develop an inexpensive, easily administered test to accurately detect and track the progression of this devastating disease. Identifying clusterin as a blood biomarker that may be relevant to both the pathology and symptoms of the disease may bring us closer to this goal," said Dr. Madhav Thambisetty, formerly of the IoP KCL UK and now with the National Institute on Aging, National Institutes of Health, US.

The authors say the results of their research add further evidence to the role of clusterin in AD, and though not a test in itself, they hope their work will lead to development of a blood test that can identify future AD victims.

"A simple blood test for detecting Alzheimer's has long been the Holy Grail for dementia researchers and these new findings edge us closer in the search. Early detection of dementia will be crucial to ensuring the treatments of the future can be given swiftly and when most effective," said Rebecca Wood, Chief Executive of the Alzheimer's Research Trust (ART). "Research is the only answer to dementia, yet our scientists remain in desperate need of funds. Investing in research now will bring the treatment breakthroughs we so urgently need in a world where 35 million live with this devastating condition."

For several years now, we've been warned of the possible dangers of cell phone use. In fact, a lawmaker in Maine wants to make her state the first to require cell phones to carry warnings that they can cause brain cancer. And San Francisco Mayor Gavin Newsom wants his city to be the nation's first to require warnings.

But -- if you will -- hold the phone for a moment. A new study in mice led by University of South Florida researchers at the Florida Alzheimer's Disease Research Center (ADRC) provides evidence that long-term exposure to electromagnetic waves associated with cell phone use may actually protect against, and even reverse, Alzheimer's disease.

"It surprised us to find that cell phone exposure, begun in early adulthood, protects the memory of mice otherwise destined to develop Alzheimer's symptoms," said lead author Gary Arendash, PhD, USF Research Professor at the Florida ADRC. "It was even more astonishing that the electromagnetic waves generated by cell phones actually reversed memory impairment in old Alzheimer's mice."

Regarding the risk of brain cancer that some researchers believe is posed by prolonged cell phone use, Arendash told ConsumerAffairs.com that the Interphone Study, which was initiated several years ago by the World Health Organization (WHO), goes a long way toward allaying such concerns.

Arendash says many of the countries that took party in that study have said independently they have found "absolutely no effects on brain cancer."

He says the claim that longer-term cell phone use doubles the risk of brain cancer needs to be put into perspective. According to Arendash, the risk of brain cancer normally is "1 in 200, so a doubling the risk is 1 in 100. That is still at or below one percent. That is still a minimal risk, even if they are correct, which I don't believe they are."

According to the study, results of which are published in the Journal of Alzheimer's Disease, exposing old Alzheimer's mice to electromagnetic waves generated by cell phones erased brain deposits of the harmful protein beta-amyloid, in addition to preventing the protein's build-up in younger Alzheimer's mice.

Sticky plaques

The sticky brain plaques formed by the abnormal accumulation of beta amyloid are a hallmark of Alzheimer's disease. Most treatments against Alzheimer's try to target beta-amyloid.

The highly-controlled study allowed researchers to isolate the effects of cell phone exposure on memory from other lifestyle factors such as diet and exercise. It involved 96 mice, most of which were genetically altered to develop beta-amyloid plaques and memory problems mimicking Alzheimer's disease as they aged. Some were non-demented, without any genetic predisposition for Alzheimer's, so researchers could test the effects of electromagnetic waves on normal memory as well.

Both the Alzheimer's and normal mice were exposed to the electromagnetic field generated by standard cell phone use for two 1-hour periods each day for seven to nine months.

The mice didn't wear tiny headsets or have scientists holding cell phones up to their ears; instead, their cages were arranged around a centrally-located antenna generating the cell phone signal. Each animal was housed the same distance from the antenna and exposed to electromagnetic waves typically emitted by a cell phone pressed up against a human head.

If cell phone exposure was started when the genetically-programmed mice were young adults -- before signs of memory impairment were apparent -- their cognitive ability was protected. In fact, the Alzheimer's mice performed as well on tests measuring memory and thinking skills as aged mice without dementia.

If older Alzheimer's mice already exhibiting memory problems were exposed to the electromagnetic waves, their memory impairment disappeared. Months of cell phone exposure even boosted the memories of normal mice to above-normal levels. The memory benefits of cell phone exposure took months to show up, suggesting that a similar effect in humans would take years if cell phone-level electromagnetic exposure were provided.

Based on their promising and unexpected findings in mice, the researchers concluded that electromagnetic field exposure could be an effective, non-invasive and drug-free way to prevent and treat Alzheimer's disease in humans. They are currently evaluating whether different sets of electromagnetic frequencies and strengths will produce more rapid and even greater cognitive benefits than those found in their current study.

A slow, chronic starvation of the brain as we age appears to be one of the major triggers of a biochemical process that causes some forms of Alzheimer's disease.

A new study from Northwestern University's Feinberg School of Medicine, published in the December 26 issue of the journal Neuron, has found when the brain doesn't get enough sugar glucose — as might occur when cardiovascular disease restricts blood flow in arteries to the brain — a process is launched that ultimately produces the sticky clumps of protein that appear to be a cause of Alzheimer's.

Robert Vassar, lead author, discovered a key brain protein is altered when the brain has a deficient supply of energy. The altered protein, called elF2alpha, increases the production of an enzyme that, in turn, flips a switch to produce the sticky protein clumps. Vassar worked with human and mice brains in his research.

"This finding is significant because it suggests that improving blood flow to the brain might be an effective therapeutic approach to prevent or treat Alzheimer's," said Vassar, a professor of cell and molecular biology at the Feinberg School.

A simple preventive strategy people can follow to improve blood flow to the brain is getting exercise, reducing cholesterol and managing hypertension.

"If people start early enough, maybe they can dodge the bullet," Vassar said. For people who already have symptoms, vasodilators, which increase blood flow, may help the delivery of oxygen and glucose to the brain, he added.

Vassar said it also is possible that drugs could be designed to block the elF2alpha protein that begins the formation of the protein clumps, known as amyloid plaques.

An estimated 10 million baby boomers will develop Alzheimer's in their lifetime, according to the Alzheimer's Association. The disease usually begins after age 60, and risk rises with age. The direct and indirect cost of Alzheimer's and other dementias is about $148 billion a year.

The initial trigger of Alzheimer's has long been a mystery.

Ten years ago, it was Vassar who discovered the enzyme, BACE1, which was responsible for making the sticky, fiber-like clumps of protein that form outside neurons and disrupt their ability to send messages.

But the cause of the high levels of the protein in people with the disease has been unknown. Vassar's study now shows that energy deprivation in the brain might be the trigger starting the process that forms plaques in Alzheimer's.

Vassar said his work suggests that Alzheimer's disease may result from a less severe type of energy deprivation than occurs in a stroke. Rather than dying, the brain cells react by increasing BACE1, which may be a protective response in the short term, but harmful in the long term.

"A stroke is a blockage that prevents blood flow and produces cell death in an acute, dramatic event," Vassar said. "What we are talking about here is a slow, insidious process over many years where people have a low level of cardiovascular disease or atherosclerosis in the brain. It's so mild, they don't even notice it, but it has an effect over time because it's producing a chronic reduction in the blood flow."

Vassar said when people reach a certain age, some may get increased levels of the enzymes that cause a build-up of the plaques. "Then they start falling off the cliff," he said.

Just in time to treat a huge increase in the aging population, British scientists say they have developed a drug that, taken daily in pill form, stops Alzheimer's disease in its tracks.

The drug is known as Rember, and scientists say it appears to be twice as effective as current Alzheimer's treatments, reducing the effects of the memory-robbing disease by as much as 81 percent. Even patients who have lost memory function appear to recover.

"We appear to be bringing the worst affected parts of the brain functionally back to life," said Dr. Claude Wischik, of the University of Aberdeen, who headed the research team.

The research was presented this week at the International Conference on Alzheimer's disease in Chicago. The trial involved more than 300 people with mild and moderate Alzheimer's disease in Britain and Singapore.

The subjects were divided into four groups, with three taking different doses of the drug and a fourth group taking a placebo After nearly a year, those with both mild and moderate Alzheimer's who were taking Rember experienced 81 per cent less mental decline compared with those on the placebo.

Those taking any dosage of the drug did not experience any significant decline in their mental function over 19 months, while those on the placebo got worse.

The drug reportedly works by targeting what are called "tangles" in the brain. These tangles are what destroy nerve cells and, over time, destroy the patient's memory function.

Currently, there is no known cure for Alzheimer's, which afflicts mostly elderly patients and eventually is fatal.

Researchers say the drug could be commercially available within four years, pending the outcome of further trials and the approval of regulatory agencies.

Today, as many as 5.2 million Americans are living with Alzheimer's disease, which includes between 200,000-500,000 people under age 65 with young-onset Alzheimer's disease or other dementias. A report by the Alzheimer's Association projects that as many as 10 million baby boomers in the U.S. will eventually develop Alzheimer's as this large demographic moves into old age.

Experts predict by 2010, there will be almost a half million new cases of Alzheimer's disease each year; and by 2050, there will be almost a million new cases each year. Eventually, the report says, the disease will strike one out of every eight boomers.

Alzheimer's disease is the seventh leading cause of death in the U.S. and the fifth leading cause of death for those over age 65.

It is one of those claims that immediately sounds too good to be true. But researchers say a new therapy, currently used to treat arthritis, appears to reverse the effects of Alzheimer's disease within minutes.

The study, published in the Journal of Neuroinflammation, details an Alzheimer's treatment based on administering a therapeutic molecule. It highlights the importance of certain soluble proteins, called cytokines, in Alzheimer's disease.

"It is unprecedented that we can see cognitive and behavioral improvement in a patient with established dementia within minutes of therapeutic intervention," said Sue Griffin, Ph.D., editor-in-chief of the journal. "It is imperative that the medical and scientific communities immediately undertake to further investigate and characterize the physiologic mechanisms involved.

"This gives all of us in Alzheimer's research a tremendous new clue about new avenues of research, which is so exciting and so needed in the field of Alzheimer's," she said.

The study focuses on one of these cytokines, tumor necrosis factor-alpha (TNF), a critical component of the brain's immune system.

Normally, TNF finely regulates the transmission of neural impulses in the brain. The authors hypothesized that elevated levels of TNF in Alzheimer's disease interfere with this regulation.

To reduce elevated TNF, the authors gave patients an injection of an anti-TNF therapeutic called etanercept. Excess TNF-alpha has been documented in the cerebrospinal fluid of patients with Alzheimer's.

"Unprecedented" effect

The authors say their study documents a dramatic and unprecedented therapeutic effect in an Alzheimer's patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine.

Etanercept (trade name Enbrel) binds and inactivates excess TNF. Etanercept is FDA approved to treat a number of immune-mediated disorders and is used off label in the study.

The use of anti-TNF therapeutics as a new treatment choice for many diseases, such as rheumatoid arthritis and potentially even Alzheimer's, was recently chosen as one of the top 10 health stories of 2007 by the Harvard Health Letter.

Similarly, the Neurotechnology Industry Organization has recently selected new treatment targets revealed by neuroimmunology (such as excess TNF) as one of the top 10 Neuroscience Trends of 2007, according to the authors. The Dana Alliance for Brain Initiatives has chosen the pilot study using perispinal etanercept for Alzheimer's for inclusion and discussion in their 2007 Progress Report on Brain Research.

The lead author of the study, Edward Tobinick M.D., is an assistant clinical professor of medicine at the University of California, Los Angeles and director of the Institute for Neurological Research, a private medical group in Los Angeles. Hyman Gross, M.D., clinical professor of neurology at the University of Southern California, was co-author.

The study is accompanied by an extensive commentary by Sue Griffin, Ph.D., director of research at the Donald W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences (UAMS) in Little Rock and at the Geriatric Research and Clinical Center at the VA Hospital in Little Rock, who along with Robert Mrak, M.D., chairman of pathology at University of Toledo Medical School, are editors-in-chief of the Journal of Neuroinflammation.

Griffin and Mrak are pioneers in the field of neuroinflammation. Griffin published a landmark study in 1989 describing the association of cytokine overexpression in the brain and Alzheimer's disease. Her research helped pave the way for the findings of the present study. Griffin has recently been selected for membership in the Dana Alliance for Brain Initiatives, a nonprofit organization of more than 200 leading neuroscientists, including ten Nobel laureates.

"Even though this report predominantly discusses a single patient, it is of significant scientific interest because of the potential insight it may give into the processes involved in the brain dysfunction of Alzheimer's."

While the article discusses one patient, many other patients with mild to severe Alzheimer's received the treatment and all have shown sustained and marked improvement, the authors say.

In a large epidemiological study, researchers found that people who drank three or more servings of fruit and vegetable juices per week had a 76 percent lower risk of developing Alzheimer's disease than those who drank juice less than once per week.

The study by Qi Dai, M.D., Ph.D., assistant professor of Medicine, and colleagues appears in the September issue of The American Journal of Medicine.

The researchers followed a subset of subjects from a large cross-cultural study of dementia, called the Ni-Hon-Sea Project, which investigated Alzheimer's disease and vascular dementia in older Japanese populations living in Japan, Hawaii and Seattle, Wash.

For the current study, called the Kame Project, the researchers identified 1,836 dementia-free subjects in the Seattle population and collected information on their dietary consumption of fruit and vegetable juices. They then assessed cognitive function every two years for up to 10 years.

After controlling for possible confounding factors like smoking, education, physical activity and fat intake, the researchers found that those who reported drinking juices three or more times per week were 76 percent less likely to develop signs of Alzheimer's disease than those who drank less than one serving per week.

The benefit appeared particularly enhanced in subjects who carry a genetic marker linked to late-onset Alzheimer's disease -- the most common form of the disease, which typically occurs after the age of 65.

The researchers chose to study this group because of the low incidence rate of Alzheimer's disease in the Japanese population. However, the incidence of Alzheimer's in Japanese people living in the United States is higher, approaching the incidence rates in Americans. This pointed to environmental factors like diet and lifestyle as important contributors to disease risk.

Originally, researchers suspected that high intakes of antioxidant vitamins might provide some protection against Alzheimer's disease, but recent clinical studies have not supported this hypothesis.

"We thought that the underlying component may not be vitamins, that there was maybe something else," Dai said.

Dai began to suspect that another class of antioxidant chemicals, known as polyphenols, could play a role. Polyphenols are non-vitamin antioxidants common in the diet and particularly abundant in teas, juices and wines.

Most polyphenols exist primarily in the skins and peels of fruits and vegetables. Recent studies have shown that polyphenols (like resveratrol in wine) extend maximum lifespan by 59 percent and delay age-dependent decay of cognitive performance in animal models.

"Also, animal studies and cell culture studies confirmed that some polyphenols from juices showed a stronger neuroprotective effect than antioxidant vitamins. So we are now looking at polyphenols," Dai said.

The next step, said Dai, is to test the subjects' blood samples to see if elevated levels of polyphenols are related to the reduced risk of cognitive decline and Alzheimer's disease. This would provide further evidence of the role of juice polyphenols in Alzheimer's disease risk. It also may point to the types of juice that would be most beneficial.

"We don't know if it is a specific type of juice (that reduces risk). That information was not collected in the current study," said Dai. "But we can use plasma to narrow down the kinds of juices."

However promising the study results appear, Dai cautioned, it's important that the general public not jump the gun regarding the value of juice as a preventive measure for Alzheimer's disease.

"A few years ago, hormone replacement therapy, NSAIDs (nonsteroidal anti-inflammatory drugs) and antioxidant vitamins showed promise (in preventing or slowing Alzheimer's disease), but recent clinical trials indicate that they do not," Dai said. "More study, I think, is needed."

A group of scientists at The Scripps Research Institute has proposed a new theory about the cause of Alzheimer's disease, the progressive neurodegenerative disorder that currently afflicts some 4.5 million Americans.

According to the hypothesis, the disease arises as a consequence of inflammation, which creates abnormal metabolites out of normal brain molecules.

These abnormal metabolites then modify "amyloid beta" proteins in the brain and cause them to misfold. Misfolded amyloid beta proteins are thought to be a major player in Alzheimer's disease, because they can accumulate into the fibrils and plaques that autopsies reveal in the brains of patients with the disease. These fibrils and plaques and their precursors are implicated in neuronal loss.

The inflammation process that creates these metabolites can be triggered by numerous stimuli, including infections that precede the onset of Alzheimer's disease by a significant amount of time -- perhaps years.

"If a certain inflammatory metabolite or family of metabolites confers risk later in life, then we need to know this, and we need to attack the problem," says Scripps Research Professor Jeffery W. Kelly, who is the Lita Annenberg Hazen Professor of Chemistry in The Skaggs Institute for Chemical Biology and vice president of academic affairs at Scripps Research.

Kelly and his Scripps Research colleagues present their new theory in an article that will be published in an upcoming issue of the journal Proceedings of the National Academy of Sciences.

Alzheimer's is a progressive neurodegenerative disease marked by memory loss, loss of language ability, loss of the ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings.

According to the Alzheimer's Disease Education and Referral Center, a service of the National Institute on Aging, Alzheimer's disease is now believed to inflict some 4.5 million people and is the most common form of dementia among older people in the United States. Currently, there is no cure for Alzheimer's and no way to slow the progression of the disease.

German doctor Alois Alzheimer discovered the disease in 1906, when he examined a post-mortem patient who had died with an unusual mental illness. Alzheimer found unusual clumps of protein or plaques in her brain. These plaquesmade up of aggregated proteins called amyloid betaare a clear sign of the disease, and the aggregation of amyloid beta protein is an accepted primary pathological marker for Alzheimer's.

But scientists have not been sure whether these fibrils are causing the disease or are simply a marker of it. By analogy, a tidal wave may cause massive destruction to a coastal area, but the tidal wave itself may have been caused by a distant earthquake undetected in that coastal area.