Evidence arises that viruses may play a role in Alzheimer's

Grant Boone
June 25, 2018

Scientists have found up to two times higher level of human herpes virus among people with Alzheimer's disease, suggesting the potential role of the viruses in the development of the progressive brain disorder. Now, according to a study conducted by researchers at the Banner Center for Neurodegenerative Disease Research at the Arizona State University, in Temple, USA, Alzheimer's disease could have a viral origin.

"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. "Our work identified specific biological networks that offer new testable hypotheses regarding the role of microbial defense and innate immune function in the pathophysiology of Alzheimer's". "But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology". While this discovery surprised the researchers, they continued to follow the path and what they learned was that the genes were "two incredibly common and closely related herpesviruses that are known to cause childhood rashes and fevers", and they are so common that nearly everyone has them.

"I don't think we can answer whether herpesviruses are a primary cause of Alzheimer's disease".

A detailed genetic analysis found that herpes viruses appear to interact with human genes previously linked to Alzheimer's, said senior author Joel Dudley.

A new study suggests that certain viruses could kick-start an immune response that might increase the accumulation of amyloid, a protein in human brains which clumps into the telltale plaques of Alzheimer's.

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Scientists have long known of an association between Alzheimer's disease and viruses, but whether that link is meaningful has been a mystery for decades.

Specifically, Alzheimer's brains had up to double the amount of HHV-6A and HHV-7 strains compared to non-Alzheimer's brains.

While the findings help potentially open the door for new therapies, nothing has fundamentally changed about how to treat Alzheimer's for now, said another of the authors Sam Gandy. In fact, in North America, approximately 90% of children have at least one of the strains in their blood in their early lives. As with any complex set of findings, they will need to be confirmed in additional patient cohorts, and further studies to specifically address a causal role for viruses are now being conducted by the research team. "It therefore doesn't change what we already know about the causes of dementia, doesn't mean that having cold sores put you at increased risk of getting it and people shouldn't be unduly anxious".

There are multiple points of overlap between virus-host interactions and genes associated with Alzheimer's risk. "It doesn't deserve to just be brushed away".

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