Published: Sat, June 23, 2018
Medicine | By Earnest Bishop

New evidence that viruses may play a role in Alzheimer's

New evidence that viruses may play a role in 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.

Alzheimer's may be triggered by a virus, according to a new study that discovered people with the disease had twice the level of the common herpes bug. But the researchers, who published their findings Thursday in the journal Neuron, emphasize that their research doesn't prove that the viruses cause the onset or progression of Alzheimer's. But we were able to do statistical causal inference testing and more sophisticated analysis, which allowed us to identify how the viruses are directly interacting with or coregulating or being regulated by Alzheimer's genes.

HAMILTON: It's not clear exactly how virus genes interact with Alzheimer's genes, but Dudley says it is clear that the same genes that make some brains more susceptible to Alzheimer's also seem to make them prone to infection with these herpes viruses.

Researchers have been attempting to identify links to viruses and, ultimately, new treatment strategies.

"We saw a key virus, HHV-6A, regulating the expression of quite a few Alzheimer's risk genes and genes known to regulate the processing of amyloid, a key ingredient in Alzheimer's neuropathology". "We didn't have a horse in this virus race whatsoever".

The researchers observed multiple viral species in the anterior prefrontal cortex and superior temporal gyrus, most notably an AD-associated increase in HHV-6A and HHV-7. Among the many challenges facing researchers is the fact that the earliest effects of the disease on vulnerable brain regions occur 20 or 30 years before memory loss, confusion, mood changes and other clinical symptoms appear.

Bryce Vissel, Professor of Neuroscience and Director, Centre for Neuroscience and Regenerative Medicine at University of Technology Sydney, said that the work is an "exceptionally important and well-executed study that presents novel evidence linking the activity of specific herpes viruses with Alzheimer's disease and offers potential new paths for disease treatment".

"All these Alzheimer's brains in these separate, major brain banks have previously unsuspected substantial populations of herpesvirus genomes and that deserves an explanation wherever it falls in the pathogenesis".

DUDLEY: Actually, a lot of well-known Alzheimer's genes came up as either interacting with the virus genes or being influenced by them.

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"We did not expect to be working on viruses", Gandy said.

HSV-1 is a different virus from HHV-6A and HHV-7, but Dudley's team did also find that Alzheimer's brains had higher than normal levels of genetic material associated with HSV-1.

"HSV wasn't one of the ones we found in the sequencing of the brain". And once the viruses get inside brain cells, they can just sit there quietly for decades until something causes them to wake up.

DUDLEY: These viruses are becoming activated, and then they put gas on the flame of the Alzheimer's pathology.

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.

About the National Institute on Aging: The NIA leads the federal government effort conducting and supporting research on aging and the health and well-being of older people. These studies combined suggest a viral contribution but have not explained how the connection works. So the Institute on Aging is funding a study that will test this approach.

"The research is not a proof of HHV involvement in Alzheimer's", he said. So Hodes says it might be possible to protect the brain with drugs that tweak the brain's immune system.

"As an illustration, we simply don't know at this point if Alzheimer's disease-related brain changes create added susceptibility to these viruses, or if infection by these viruses creates additional risk of Alzheimer's disease".

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