Childhood virus HHV linked with Alzheimer's decades later

Seven local musicians volunteered their talent for the event

New research by a team of scientists in Waterford has identified a unique combination of nutrients that they say slows the progression of Alzheimer's disease.

Some scientists have long suspected viruses or bacteria somehow set the stage for Alzheimer's. According to the so-called pathogen hypothesis of AD, the brain reacts to infection by engulfing viruses with the protein amyloid beta (Aβ), sequestering the invaders and preventing them from binding with cell surfaces and inserting their viral genetic payload into healthy cells.

The new research is the fruitful result of close working relationships among researchers from Arizona State University, Banner, Mount Sinai and other research organizations, as well as public-private partnerships in AMP-AD.

For the new study, which was broadly created to map and compare genetic, transcriptional, and protein networks underlying AD, the team analyzed whole exome DNA and RNA sequencing data from 622 brain donors with early- and later-stage clinical and neuropathological features of AD, and another 322 brains from donors without the disease, generated through the National Institutes of Health (NIH)-sponsored Accelerated Medicines Partnership for Alzheimer's Disease (AMP-AD). Dudley has met researchers at conferences who have confided in him that they have also collected data implicating pathogens in the disease but that they have been too scared to publish-for fear that they will be ostracized by the Alzheimer's community.

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Joel Dudley, director of the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai and the paper's senior author, said the study could potentially translate to the identification of virus, or virus-related, biomarkers that could improve patient risk stratification and diagnosis.

The study, using evidence from post-mortem brain tissue, was carried out by researchers from Mount Sinai Health System in NY in the US. They constructed, mapped, and compared regulatory gene networks in areas of the brain known to be affected by Alzheimer's on multiple levels, looking at DNA, RNA, and proteins.

Streetman says there are 34,000 people age 65 or older living with Alzheimer's in the state - and roughly 82,000 people providing uncompensated care. But it was never clear if germs were merely bystanders, or actively spurring Alzheimer's.

Streetman says the fundraising helps support the Alzheimer's Association's many programs and services. "We were able to use a range of network biology approaches to tease apart how these viruses may be interacting with human genes we know are relevant to Alzheimer's".

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And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's. To see if those interactions mattered, the researchers bred mice lacking one molecule that herpes seemed to deplete. More evidence is accumulating to indicate that this loss of cognitive functioning is a mix of many different disease processes in the brain, rather than just one, such as buildup of amyloid or tau proteins. "It shows that there is a link", said Keith Fargo, scientific director of the Alzheimer's Association, who was not involved in the work.

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

If the findings eventually pan out, they could lead to new targets for Alzheimer's treatment. In February 2018, Taiwanese researchers reported that individuals infected with herpes simplex virus 1 (HSV-1), the virus that causes cold sores, were 90 percent less likely to develop senile dementia than infected people who weren't treated if they received treatment with antiviral drugs. The plaques also alert brain immune cells called microglia to the fact that something is wrong; these cells launch an immune cascade that kills even more neurons.

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