Herpes may play role in pathogenesis of Alzheimer’s

Herpes virus present within the body long after the overt infection may play a role in the pathogenesis of Alzheimer’s disease say researchers. The study titled, “Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus” appeared in the latest issue of the journal Neuron, this Thursday.

Human Herpes simplex virus 3D illustration. Image Credit: Kateryna Kon / SHutterstock
Human Herpes simplex virus 3D illustration. Image Credit: Kateryna Kon / Shutterstock

For this latest study the team of researchers looked at the brain tissues donated after their deaths by 622 individuals with Alzheimer’s disease and 322 people who did not have Alzheimer’s disease. Results from the analysis revealed that specific herpes viruses were found more commonly in brains of people with Alzheimer’s disease. HHV-6A and HHV-7 – the two herpes viruses were found more frequently than others in brains of people who had Alzheimer’s disease.

There have been earlier studies hypothesizing that viral infections could be the key to Alzheimer’s disease. HSV-1 for example – one that causes cold sores – has been studied in neurodegenerative diseases.  Sam Gandy, senior author of this study and Alzheimer’s disease specialist at the Ichan School of Medicine at Mount Sinai said that anti-HSV-1 antibodies have been studied in these patients earlier. Presence of these antibodies indicated the encounters of the person with this virus sometime during their lives. This new study, he explained showed -V6 and HHV-7 viral genes within the brains of persons with Alzheimer’s after they had died.

Ben Readhead, the study’s lead author said that the purpose of the study was to find ways to understand the disease and treat it better. The viral genes were a chance finding that was so significant that they had to be reported, he said. They tested the brain samples from the Mount Sinai Brain Bank, he said and were so surprised at the finding that they tested additional samples from other brain banks and found same results. Joel Dudley, one of the authors and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mt. Sinai, said this was “gas to the flame” of what we already knew about the viral connection with Alzheimer’s disease. He explained that like many other scientific experiments. This was an accidental finding. Gandy said that the Alzheimer’s genes were apparently being “modulated” by the HHV6/7 and so it could be the viral proteins that could be turning on the genes responsible for Alzheimer’s disease.

Researchers say that both of these viruses are very common and almost all individuals over the age of six have at least one of the two circulating in their blood. The viruses remain dormant however within the body. Readhead said the connection between finding the virus in the blood and it activating the Alzheimer’s genes and triggering the disease is still not understood well. Gandy also said these findings could open new avenues of research for treatment of the disease but at present risk susceptibility for the disease is still not clearly understood. For this more detailed future studies are necessary, they agree.

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