Study linking herpes and Alzheimer’s rekindles debate over controversial old hypothesis

Study linking herpes and Alzheimer’s rekindles debate over controversial old hypothesis

This work lends support to the controversial hypothesis that viruses are involved in Alzheimer's disease and offers potential new paths for treatment. The researchers also identified a microRNA- a short molecule that typically switches genes off-that is suppressed by the HHV-6A virus in Alzheimer's brains. The research doesn't prove anything just yet, but it's an interesting theory and one that many experts have been talking about for some time.

The Longest Day is one the biggest fundraising days for The Alzheimer's Association and is a way for them to raise money for programs, research, and education.

These herpes viruses are extremely common, and can cause a skin rash called roseola in young children.

But new research has found the brains of people who have died of Alzheimer's have nearly double the level of HHV-6A and HHV-7 herpes virus, as non-diseased brains, suggesting it is playing a role in the condition.

Viruses could play a key role in the development of Alzheimer's disease, a new study suggests.

Some scientists have long suspected viruses or bacteria somehow set the stage for Alzheimer's. Multiscale analysis of independent Alzheimer's cohorts finds disruption of molecular, genetic, and clinical networks by human herpesvirus [published online June 21, 2018].

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Currently, no effective prevention or treatment exists for this progressive deterioration of brain tissue, memory and identity, but researchers are hopeful that new, better treatments can emerge as a result of their work. "This research reinforces the complexity of Alzheimer's disease, creates opportunities to explore Alzheimer's more thoroughly, and highlights the importance of sharing data freely and widely with the research community".

"Previous studies of viruses and Alzheimer's have always been very indirect and correlative", states Joel Dudley, Ph.D., associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mount Sinai and associate research professor at the Arizona State University-Banner Neurodegenerative Disease Research Center (NDRC). "HHV-6A stood out as a notable", they state, and exhibited a significant overlap between the set of host genes it collectively induced across all tissues and AD-associated genes. It seems feasible that amyloid is not the cause of disease in many cases. Further study into how these particular viruses interacted with human genes revealed they may disrupt a gene galled Mir155. "And if viral infections are playing a part, they are not the sole actor". The constructed virus-host protein networks also suggested that herpesvirus interaction perturbed cell nucleotide pools, tRNA synthesis, and protein translation, "which suggested a picture of virally induced dysregulation of nucleotide pool metabolism, especially purine bases, consistent with several metabolomics studies in AD".

And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's. Most abundant were two human herpes viruses, known as HHV6a and HHV7, that infect most people during childhood, often with no symptoms, and then lie dormant in the body. "We were looking for genes that were dysregulated during the progression of Alzheimer's disease".

Study author Professor Dr Sam Gandy added: "This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer's".

"This opens up the door for looking for new therapies that target the immune system in Alzheimer's", Dudley said.

The researchers believe that their findings align with other current research in the Alzheimer's field on the role of innate immunity in the disease, particularly recent findings that beta-amyloid protein-the culprit behind the plaques that build up in the Alzheimer's-affected brain-may accumulate as part of a defense against infections.

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