Irish 'breakthrough of the century' on Alzheimer's disease

Grant Boone
June 23, 2018

A robust and sophisticated new study has now exploded onto the scene, rekindling the viral hypothesis for Alzheimer's through an accidental discovery. They infect almost every human, typically during infancy, and have been closely linked to the childhood rash called roseola, according to the HHV-6 Foundation. 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 study points to the viruses as possible accomplices that drive disease progression but does not suggest that Alzheimer's may begin after they are transmitted through casual contact.

But a team led by researchers at New York's Mount Sinai Health System found that certain viruses - including two extremely common herpes viruses - affect the behavior of genes involved in Alzheimer's.

Studies have previously suggested that viruses might be linked with Alzheimer's but the new research suggests a relationship between viruses and the activity of genes associated with the disease.

Some scientists have long believed that viruses play a role in the development of Alzheimer's.

They found that human herpesvirus 6A and 7 were up to twice as abundant in Alzheimer's disease samples than non-Alzheimer's ones. "It shows that there is a link", said Keith Fargo, scientific director of the Alzheimer's Association, who was not involved in the work.

He and a team of researchers were using genetic data to look for differences between healthy brain tissue and brain tissue from people who died with Alzheimer's. Instead, what ultimately stood out to them were not any particular human genes but in fact an abundance of genes related to two particular strains of herpes virus. 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.

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. "Collectively, these findings support the role of miR-155 as a key node in host response to AD-relevant viral perturbation, and as a potential mediator of neuronal loss", they state.

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The investigators found that the Alzheimer's disease process is likely affected by a complex series of interactions between viral and human genetics.

"The title of the talk that I usually give is, 'I Went Looking for Drug Targets and All I Found Were These Lousy Viruses, '" explains Joel Dudley, co-senior author on the study. "We saw a key virus, HHV-6A, regulating the expression of quite a few AD risk genes and genes known to regulate the processing of amyloid, a key ingredient in AD neuropathology".

HSV-1 is a different virus from HHV-6A and HHV-7, but Dudley's team did also find that Alzheimer's brains had higher than normal levels of genetic material associated with HSV-1.

The findings were based on RNA sequencing on four brain regions in more than 600 samples of postmortem tissue from people with and without Alzheimer's.

Although the hypothesis that viruses play a part in brain disease isn't new, "this is the first study to provide strong evidence based on unbiased approaches and large datasets that lends support to this line of inquiry", comments NIA director Richard J. Hodes, M.D.

"If it becomes evident that specific viral species directly contribute to an individual's risk of developing Alzheimer's or their rate of progression once diagnosed, then this would offer a new conceptual framework for understanding the emergence and evolution of Alzheimer's at individual, as well as population, levels". Now, the main theory is that sticky brain-clogging plaques are the culprit.

"When we celebrate this, because we are celebrating our caregivers, we are recognizing there is a need for research of Alzheimer's, and at the end of the day, we know we did a great thing by bringing awareness to the cause", said Sheila Hutcherson, President, Gamma Sigma Omega Chapter.

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