New evidence that viruses may play a role in Alzheimer's National News


New evidence that viruses may play a role in Alzheimer's National News

Henrietta Brewer
June 23, 2018

Thanks to a new NIH-led public-private partnership called the Accelerating Medicines Partnership - Alzheimer's Disease (AMP-AD), the team had access to data from 876 brains-some healthy and some with early- or late-stage Alzheimer's.

The researchers from the Nutrition Research Centre of Ireland say that the study has yielded a "statistically significant" finding and have described it as a "breakthrough". "However, if viruses or other infections are confirmed to have roles in Alzheimer's, it may enable researchers to find new anti-viral or immune therapies to treat or prevent the disease". Rather, the research gives scientists reason to revisit the old pathogen hypothesis and will be the basis for further work that will test whether herpes virus activity is one of the causes of Alzheimer's.

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.

"The hypothesis that viruses play a part in brain disease is not new, but this is the first study to provide strong evidence based on unbiased approaches and large data sets that lends support to this line of inquiry", said NIA Director Richard J. Hodes, M.D.

The idea that microbes and viruses may somehow contribute to the onset and progression of AD has been mooted for at last 60 years, but studies have yet to generate definitive evidence, the authors explain.


The study found that herpes viruses were involved in networks that regulate amyloid precursor proteins.

"The research is not a proof of HHV involvement in Alzheimer's", he said. 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.

The research group, including experts from Icahn School of Medicine at Mount Sinai and Arizona State University, performed RNA sequencing on four brain regions in more than 600 samples of postmortem tissue from people with and without Alzheimer's to quantify which genes were present in the brain. 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.

They found a lot of interactions, suggesting the viruses could even switch on and off Alzheimer's-related genes.

And those with more advanced disease had more virus in their brains.


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 brain is shown here as a complex network of interactions, with disruption of connections by the key viral species (HHV-6A, HHV-6B, HHV-7) identified in this study.Ben Readhead et al.

They also found that these Alzheimer's risk genes seem to make a person's brain more vulnerable to infection with the two herpes viruses.

"This study illustrates the promise of leveraging human brain samples, emerging big data analysis methods, converging findings from experimental models, and intensely collaborative approaches in the scientific understanding of AD and the discovery of new treatments", adds study co-author Eric Reiman, M.D., executive director of the Banner Alzheimer's Institute and University Professor of Neuroscience at Arizona State University.

Alzheimer's disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks.

Streetman says the fundraising helps support the Alzheimer's Association's many programs and services.


Around 850,000 people are living with dementia in Ireland and Britain, and the majority of people have Alzheimer's which occurs when sticky plaques of amyloid build up in the brain, killing brain cells.

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