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.”
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.