A provocative new study says viruses that sneak into the brain just might play a role in Alzheimer's.
The idea that microbes and viruses may somehow contribute to the onset and progression of AD has been mooted for at last 60 years, but studies have yet to generate definitive evidence, the authors explain.
The researchers believe that their findings align with other current research in the Alzheimer's field on the role of innate immunity in the disease, particularly recent findings that beta-amyloid protein-the culprit behind the plaques that build up in the Alzheimer's-affected brain-may accumulate as part of a defense against infections.
That wasn't unusual. Since 1980, other researchers have linked a variety of bacteria and viruses, including another type of herpes that causes cold sores, to an increased risk of Alzheimer's.
The research group, which included experts from Icahn School of Medicine at Mount Sinai, New York City, and Arizona State University, Phoenix, originally set out to find whether drugs used to treat other diseases can be repurposed for treating Alzheimer's.
If the findings pan out, they could change how scientists look for new ways to treat or prevent Alzheimer's, said Dr. Miroslaw Mackiewicz of NIH's National Institute on Aging.
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"What we found was that the most dysregulated sequences were not from the brain itself, but from the genomes of HHV-6A and HHV-7", he added.
"Previous studies of viruses and Alzheimer's have always been very correlative".
The research community has been seeking new insights into the pathology of Alzheimer's because decades of research and hundreds of failed clinical trials have only resulted in disagreements about its underlying biology-and no new treatments have emerged to modify the course of the memory-robbing disease. The study points to the viruses as possible accomplices that drive disease progression but does not suggest that Alzheimer's may begin after they are transmitted through casual contact.
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.
And those with more advanced disease had more virus in their brains. They infect almost every human, typically during infancy, and have been closely linked to the childhood rash called roseola, according to the HHV-6 Foundation. "It shows that there is a link", said Keith Fargo, scientific director of the Alzheimer's Association, who was not involved in the work.
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Although the hypothesis that viruses play a part in brain disease isn't new, "this is the first study to provide strong evidence based on unbiased approaches and large datasets that lends support to this line of inquiry", comments NIA director Richard J. Hodes, M.D.
Officials tell News 10 that every 65 seconds someone in the U.S.is diagnosed with Alzheimers. "This is is also consistent with the contribution of viral perturbation in driving the preclinical AD transcriptional phenotype, given that our prioritization of miR-155 was informed by findings in the preclinical AD networks". The plaques also alert brain immune cells called microglia to the fact that something is wrong; these cells launch an immune cascade that kills even more neurons.
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. And now, not only is the viral hypothesis resurrected: "it has specific testable pathways and networks and interactions that can be explored and reconciled with the rest of the work emerging in Alzheimer's", says Dudley.
But Dudley is willing to accept the risks and push forward.
"We didn't go looking for viruses, but viruses sort of screamed at us", states lead author Ben Redhead, assistant research professor at the NDRC. "But the data are the data".
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