Sunday, 22 July, 2018

High-level viruses found in Alzheimer's disease brain

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Brains riddled with Alzheimer's disease contain high levels of two strains of human herpes virus, researchers discovered. While a group of dedicated scientists continued to toil away at investigations correlating viral infections with Alzheimer's, the general research community began to focus on the amyloid hypothesis as the fundamental causal explanation behind the disease.

The researchers were funded by the National Institute on Aging of the National Institutes of Health.

More on this research is available in announcements from the Icahn School of Medicine at Mount Sinai, Arizona State University and Cell Press, the publisher of Neuron.

And like other herpes viruses, it can flare up after having been dormant for decades.

"We didn't set out to find what we found".

"To be clear, it does not prove the idea that viruses causes Alzheimer's".

Joel Dudley, director of the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai and the paper's senior author, said the study could potentially translate to the identification of virus, or virus-related, biomarkers that could improve patient risk stratification and diagnosis. Comparisons between AD and other neuropathological controls, enabled through inclusion of one particular dataset, suggested that "HHV-6A and HHV-7 are not ubiquitous features of neuropathology and appear at least partially specific to AD", the researchers comment.

The study found that herpes viruses were involved in networks that regulate amyloid precursor proteins. Their theory posits that when enough beta amyloid plaques build up during an infection, they then trigger inflammation and other unhelpful responses, such as the creation of tau tangles that kill neurons.

As Readhead explained, "A number of viruses looked interesting".

And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's. Most people are exposed to them early in life.

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The results from human brain tissue were further supplemented by mouse studies. As the authors note, HHV 6A is known to deplete miR155, lending further weight to a viral contribution to AD.

"Our work identified specific biological networks that offer new testable hypotheses regarding the role of microbial defence and innate immune function in the pathophysiology of Alzheimer's".

"This study illustrates the promise of leveraging human brain samples, emerging big data analysis methods, converging findings from experimental models, and intensely collaborative approaches in the scientific understanding of AD and the discovery of new treatments", adds study co-author Eric Reiman, M.D., executive director of the Banner Alzheimer's Institute and University Professor of Neuroscience at Arizona State University.

A robust and sophisticated new study has now exploded onto the scene, rekindling the viral hypothesis for Alzheimer's through an accidental discovery.

In the meantime, Alzheimer's continues its devastating trajectory. Recent research has also implicated viruses in the development of Parkinson's disease and amyotrophic lateral sclerosis (ALS).

A provocative new study says viruses that sneak into the brain just might play a role in Alzheimer's.

"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.

Dudley and his colleagues stumbled across this possible viral link to Alzheimer's during an analysis meant to find ways that drugs used to treat other illnesses could be repurposed for treating the dreaded neurodegenerative disease.

HAMILTON: Joel Dudley is an associate professor at the Icahn School of Medicine at Mount Sinai in NY.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services.

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