Alzheimer's may be triggered by herpes virus

GETTY ImagesDementia Maintaining a healthy lifestyle could lower your risk of Alzheimer's

Although the findings did not prove that the viruses directly cause its onset or progression, they have showed the viral DNA sequences and the activation of biological networks may interact with molecular, genetic and clinical aspects of Alzheimer's, according to the study.

In this study, researchers initially performed RNA sequencing on more than 600 samples of postmortem tissue of people with and without Alzheimer's, looking to quantify which genes were present in the brain and whether any were associated with the development of the disease. "It could be that things are not as binary as we thought, that viruses act one way and genes another". 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. I don't think we can answer whether herpesviruses are a primary cause of AD. "But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology", says Dudley.

The study found that herpes viruses were involved in networks that regulate amyloid precursor proteins. "Whether such findings represent a causal contribution, or reflect opportunistic passengers of neurodegeneration, is also hard to resolve". Each patient had undergone clinical evaluation to follow the course of their disease before death and neuropathological evaluation to evaluate factors, including the degree of amyloid plaque formation.

The goal was to identify new targets for drugs.

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. The researchers also identified a microRNA- a short molecule that typically switches genes off-that is suppressed by the HHV-6A virus in Alzheimer's brains.

The two viruses they found to be most strongly associated with Alzheimer's, HHV-6A and HHV-7, were not as abundant in the brains of those with other neurodegenerative disorders.

"We found prominent roles for Roseoloviruses HHV-6A and HHV-7, both implicated across multiple domains, and 3 independent cohorts", the team writes.

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Researchers said previous studies suggest a viral contribution but don't explain how the connection works.

The nature and significance of viruses and other pathogens in the brain are now hot topics in neuroscience, though the exploration is still in its early stages. Instead, what ultimately stood out to them were not any particular human genes but in fact an abundance of genes related to two particular strains of herpes virus.

"We didn't go looking for viruses, but viruses sort of screamed out at us", said lead author Ben Readhead, of Arizona State University. "It could be that viruses act through genes".

And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's.

The researchers were particularly interested in the microRNA (miRNA) miR-155, which has previously been linked with neuropathologic features of AD. "And if viral infections are playing a part, they are not the sole actor". Antiviral drugs could also be explored as a potential preventive treatment.

"While these findings do potentially open the door for new treatment options to explore in a disease where we've had hundreds of failed trials, they don't change anything that we know about the risk and susceptibility of Alzheimer's disease or our ability to treat it today", says co-senior author and Alzheimer's disease specialist Sam Gandy. "We are excited about the chance to capitalize on this approach to help in the scientific understanding, treatment, and prevention of Alzheimer's and other neurodegenerative diseases".

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