Herpesvirus may contribute to Alzheimer's development, researchers say

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The team found that levels of two human herpes viruses, HHV-6 and HHV-7, were up to twice as high in brain tissue from people with Alzheimer's.

"While the findings indicate a link between the activity of these viruses and Alzheimer's, they don't tell us whether they contribute to the development of the disease, help the brain to cope with the disease, or just occur alongside Alzheimer's-processes without having an impact on the health of the brain", says David Reynolds, Chief Scientific Officer of Alzheimer's Research UK.

Researchers at the Icahn School of Medicine in NY and Arizona State University in Tempe conducted RNA sequencing on data from 3 brain banks to evaluate differential viral abundance in AD.

A study published on Thursday in the journal Neuron revealed that human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) might play a role in regulatory genetic networks that are believed to lead to the brain disease.

The two viruses they found to be most strongly associated with Alzheimer's, HHV-6A and HHV-7, were not as abundant in the brains of those with other neurodegenerative disorders. HHV six and seven are fairly common in young kids and can cause what's known as sixth disease with a fever and rash.

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The team found viral genetic material at far higher levels in Alzheimer's-affected brains than in normal ones.

"The title of the talk that I usually give is, "I Went Looking for Drug Targets and All I Found Were These Lousy Viruses", says co-senior author and geneticist Joel Dudley. who is also a member of the ASU-Banner Neurodegenerative Disease Research Center. "We were able to use a range of network biology approaches to tease apart how these viruses may be interacting with human genes we know are relevant to Alzheimer's".

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".

"However many scientists, including myself, have been concerned by the failures of recent large trials of drugs that have been developed to remove amyloid from the brain, and we have therefore focused on alternative thinking". By looking at the brain, the researchers got a better idea of whether the viruses were affecting the brain.

The study also fits with mounting evidence that how aggressively the brain's immune system defends itself against viruses or other germs may be riskier than an actual infection, said Alzheimer's specialist Dr. Rudolph Tanzi of Massachusetts General Hospital. Observations were then verified using datasets from the Religious Orders Study, the Memory and Aging Project, and the Mayo Clinic Brain Bank. 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 AD.

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DUDLEY: Actually, a lot of well-known Alzheimer's genes came up as either interacting with the virus genes or being influenced by them. The brain is shown here as a complex network of interactions, with disruption of connections by the key viral species (HHV-6A, HHV-6B, HHV-7) identified in this study.Ben Readhead et al.

Prof Dudley said: "We didn't have a horse in this virus race whatsoever".

For more information on going purple for "The Longest Day", or for resources for families with Alzheimer's, head to the Alzheimer's Association's website here.

Professor John Nolan, who led the study, said that their previous work confirmed that carotenoids are found in the eye and that enrichment of these essential nutrients with nutritional supplements can improve visual function. Richard Hodes directs the National Institute on Aging, which helped pay for the research.

Blue Cross Blue Shield of MI and the Alzheimer's Association have asked various MI landmarks to "Go Purple"-including the 9&10 News Heritage House Station Thursday evening". These herpes viruses appear to trigger an immune response in the brain that can accelerate the disease.

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