Alzheimer's could be linked to common childhood viruses, researchers say

Alzheimer's could be linked to common childhood viruses, researchers say

Reporting in the June 21 issue of the journal Neuron, the authors emphasize that their findings do not prove that the viruses cause the onset or progression of Alzheimer's.

The team found viral genetic material at far higher levels in Alzheimer's-affected brains than in normal ones. "But what's clear is that they're perturbing and participating in networks that directly underlie Alzheimer's pathophysiology".

The finding adds credence to a decades-old idea that an infection can cause Alzheimer's disease. It raises hopes that cases could be prevented through antiviral drugs. This analysis allowed us to identify how the viruses are directly interacting with or coregulating known Alzheimer's genes.

"The data are very provocative, but fall short of showing a direct causal role", he says.

The scientists caution that people shouldn't be alarmed by their discovery.

Researchers say their findings suggest that a controversial hypothesis that viruses are involved in dementia may be correct.

About AMP-AD: The Accelerating Medicines Partnership is a joint venture among the National Institutes of Health, the Food and Drug Administration, 12 biopharmaceutical and life science companies and 13 non-profit organizations, managed by the Foundation for the NIH, to identify and validate promising biological targets of disease.

"We didn't have a horse in this virus race whatsoever", says Dudley.

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In a study, the virus was found to be more prominent in the brains of people who've died with Alzheimer's Disease. The team profiled sample transcriptomes across 4 brain regions - superior temporal gyrus (n=137), anterior prefrontal cortex (n=213), inferior frontal gyrus (n=186), and parahippocampal gyrus (n=107) - from a primary cohort of individuals with AD and controls from the Mount Sinai Brain Bank in order to measure the existence and abundance of 515 viral species that infect humans as a primary host. The viruses can cause high fevers and rashes. They analyzed gene sequences taken from the brains - both genes of the patients and of any viruses that happened to be in their brains. He says The Longest Day is all about love - doing something to show love for those affected by Alzheimer's Disease.

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.

"We were able to build a social network of the virus and the host genes, to see who is friends with who", Dudley said. In essence, he says, they wanted to know: "If the viruses are tweeting, who's tweeting back?" So, while the connection found in this research is intriguing, it can not draw a clear line between the presence of the virus and the onset of Alzheimer's. Something needs to activate the viruses, which causes them to begin replicating. It's been overshadowed by the prevailing theory that Alzheimer's stems from sticky plaques that clog the brain. "They are sort of throwing a wrench in the works", he says. 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.

Previous studies that implicated the cold sore virus (HSV-1) and other viruses in Alzheimer's only looked at blood. Comparisons between AD and other neuropathological controls, enabled through inclusion of one particular dataset, suggested that "HHV-6A and HHV-7 are not ubiquitous features of neuropathology and appear at least partially specific to AD", the researchers comment.

Even so, Hodes is optimistic.

Bryce Vissel, Professor of Neuroscience and Director, Centre for Neuroscience and Regenerative Medicine at University of Technology Sydney, said that the work is an "exceptionally important and well-executed study that presents novel evidence linking the activity of specific herpes viruses with Alzheimer's disease and offers potential new paths for disease treatment".

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