Published: Fri, June 22, 2018
Medical | By Marta Holmes

More evidence for controversial theory that herpesviruses play role in Alzheimer's disease

More evidence for controversial theory that herpesviruses play role in Alzheimer's disease

Now, the main theory is that sticky brain-clogging plaques are the culprit. With Harvard colleague Dr. Robert Moir, Tanzi has performed experiments showing that sticky beta-amyloid captures invading germs by engulfing them - and that's why the plaque starts forming in the first place.

One of the primary questions is whether such pathogens play an active, causative role in the disease or enter the brain simply as opportunistic passengers, taking advantage of the neural deterioration characteristic of Alzheimer's disease. Dudley has met researchers at conferences who have confided in him that they have also collected data implicating pathogens in the disease but that they have been too scared to publish-for fear that they will be ostracized by the Alzheimer's community.

"This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer's", said study co-author Dr. Sam Gandy, a professor of neurology and psychiatry and director of the Center for Cognitive Health at Mount Sinai in NY.

About AMP-AD: The Accelerating Medicines Partnership is a joint venture among the National Institutes of Health, the Food and Drug Administration, 12 biopharmaceutical and life science companies and 13 non-profit organizations, managed by the Foundation for the NIH, to identify and validate promising biological targets of disease.

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The findings were based on a large-scale analysis at three different brain banks by researchers from the Icahn School of Medicine at Mount Sinai and Arizona State University-Banner Neurodegenerative Disease Research Center (NDRC).

Dr David Reynolds, chief scientific officer at Alzheimer's Research UK, said the viruses highlighted in the study were not the same as those that caused cold sores.

The investigators found that the Alzheimer's disease process is likely affected by a complex series of interactions between viral and human genetics. Identifying links to viruses may help researchers learn more about the complicated biological interactions involved in Alzheimer's, and potentially lead to new treatment strategies.

They say, "It'll be a day filled with sweet visuals of local seniors engaging with the community to support their peers affected by Alzheimer's". But it was never clear if germs were merely bystanders, or actively spurring Alzheimer's.

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But even if questions remain, this research offers strong support for a long-controversial hypothesis that viruses might be involved in the development of Alzheimer's disease.

"We were able to build a social network of the virus and the host genes, to see who is friends with who", Dudley said. The viruses "seemed to be talking to some of the networks that contained some of the familiar Alzheimer's-related genes". When they later bred mice deficient in this microRNA, they found that the rodents developed larger and more abundant amyloid plaques in their brains than did mice with normal microRNA levels.

Sam Gandy, professor of neurology and psychiatry, and co-author of the study, said: "This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer's".

One is to give antiviral drugs to people with high levels of herpes virus in their brains.

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Just having a herpes virus "does not mean you're going to get Alzheimer's", Mass General's Tanzi stressed. Those efforts have failed to improve brain function even when they accomplished their immediate goal. They began their direct investigation of viral sequences using data from the Mount Sinai Brain Bank and were able to verify their initial observations using datasets from the Religious Orders Study, the Memory and Aging Project and the Mayo Clinic Brain Bank.

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