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.
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.