New Evidence That Viruses May Play A Role In Alzheimer’s

Prof Riona Mulcahy and Prof John Nolan

Prof Riona Mulcahy and Prof John Nolan

"The more we learn about the disease process and the more targets we can address", he says, "the greater the probability we are going to slow or prevent the progression of Alzheimer's disease".

"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.

A new study from a team at the Icahn School of Medicine at Mount Sinai has revealed an unexpected correlation between Alzheimer's disease and high levels of human herpes virus DNA.

The researchers analyzed data from three major brain banks courtesy of the National Institutes of Health's Accelerating Medicines Partnership - Alzheimer's Disease (AMP-AD) consortium, which allowed them to look at raw genomic data for large numbers of Alzheimer's patients in different cohorts.

"We were able to build a social network of the virus and the host genes, to see who is friends with who", Dudley said.

"We didn't have a horse in this virus race whatsoever", says Dudley. Science is now helping us understand exactly what nutrients our brains need. 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.

The researchers confirmed their findings with sequencing samples collected by other brain banks, including the Mayo Clinic in Florida and the Religious Orders Study at Rush University in Chicago, observing a persistent abundance of HHV-6A and HHV-7 among Alzheimer's disease patients in those cohorts, too.

Childhood viruses that infect nearly everyone and lie dormant in the body for life might be involved in Alzheimer's disease, researchers reported Thursday.

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. "'But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology". It's been overshadowed by the prevailing theory that Alzheimer's stems from sticky plaques that clog the brain. What they found is that Alzheimer's biology is likely impacted by a complex constellation of viral and host genetic factors, adding that they identified specific testable pathways and biological networks.

They argue, however, that their work shouldn't make anyone anxious.

While the current findings are more specific, they do not provide evidence to change how risk and susceptibility are assessed, nor the diagnosis and treatment of Alzheimer's, the authors said.

This is especially true because HHV-6A and HHV-7 are extremely common and often latent or asymptomatic: in North America, nearly 90% of children have one of these viruses circulating in their blood by the time they're a few years old. 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. "But it would be negligent for us to ignore these results until the next study reports back, which will take several years".

The study, by scientists at Waterford Institute of Technology (WIT) in conjunction with others from Cambridge University, has been hailed by one researcher as "one of the most important medical advancements of the century". Note: material may have been edited for length and content.

Alzheimer's groups have used this day to bring awareness to the disease. "This is the first study to provide evidence based on multiple, large data sets that lends support to this idea". Incorporating data from the Emory Alzheimer's Disease Research Center provided insight into viral impact on proteins.

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