Herpes virus may play role in Alzheimer's, study says

These Slices of Human Brains Revealed an Alzheimer's Clue

One of the most prominent theories is that Alzheimer's may start in the brain as a response to injury from a virus. While this discovery surprised the researchers, they continued to follow the path and what they learned was that the genes were "two incredibly common and closely related herpesviruses that are known to cause childhood rashes and fevers", and they are so common that nearly everyone has them.

Results of the study were published online in Neuron on June 21.

What the study looks like, is that the herpes virus interacts with molecular "pathways" as well as with Alzheimer's risk genes. That meant identifying interactions between the virus genes and other genes in brain cells.

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Specifically, Alzheimer's brains had up to double the amount of HHV-6A and HHV-7 strains compared to non-Alzheimer's brains. By mid-century, a new diagnosis will occur every 33 seconds, and costs are expected to exceed $1 trillion annually. The study's authors pored over DNA and RNA sequencing data from 622 brains donated by people affected by Alzheimer's and 322 brains that were free of the disease.

Using different computational approaches, the team uncovered a complex network of unexpected associations, linking specific viruses with different aspects of Alzheimer's biology. The combined funding support for this five-year endeavor is $185.2 million.

Readhead and his team of researchers were not looking for the possible viruses but were only seeking to find networks of the brain upon which the current drugs could be repurposed to focus on potential treatments for the disease. "These viruses are probably significant players in driving the immune system in Alzheimer's", Joel Dudley of the Icahn School of Medicine and senior author of the study, tells Belluck.

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The theory that viruses could contribute to the development of dementia arose in the 1950s.

Dudley notes that this study could potentially translate to the identification of virus, or virus-related, biomarkers that could improve patient risk stratification and diagnosis, as well as implying novel viral targets and biological pathways that could be addressed with new preventative and therapeutic drugs.

"Similar to other studies in this area, while this is robust research, it could not prove that the viruses actually were responsible for the disease", said James Pickett, the head of research at Alzheimer's Society. Considering how finding a way to detect the disease early as well as treatment to stop the progression or even reverse it has eluded researchers, any new ideas are encouraging and can bring much-needed hope where there hasn't been much previously. "A similar situation arose recently in certain forms of Lou Gehrig's disease".

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Exploring the significance of viruses in the brain is still at its early stages, and a key question is whether pathogens play an active role in causing disease or are opportunistic, taking advantage of neural deterioration.

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