Health Care

Fight to end Alzheimer's on The Longest Day

Fight to end Alzheimer's on The Longest Day”

American researchers found that two strains of human herpesvirus were found in the brains of people with Alzheimer's disease at levels up to twice as high as in those without Alzheimer's. "But we were able to perform a more sophisticated computational analysis using multiple levels of genomic information measured directly from affected brain tissue".

Childhood viruses that infect nearly everyone and lie dormant in the body for life might be involved in Alzheimer's disease, researchers reported Thursday. They then found evidence that the viruses influence the behaviour of genes involved in Alzheimer's.

Over the last few years, though, after a series of failed clinical trials into drugs created to attack amyloid plaque build-ups, a growing community of researchers has resurrected this old hypothesis.

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.

"The more we learn about the disease process and the more targets we can address", he says, "the greater the probability we are going to slow or prevent the progression of Alzheimer's disease". The researchers initially set out to comprehensively examine DNA, RNA and protein footprints in the brains of deceased Alzheimer's patients with the goal of identifying certain overactive genes in Alzheimer's sufferers that could help direct future drug research.

"We saw a key virus, HHV-6A, regulating the expression of quite a few Alzheimer's risk genes and genes known to regulate the processing of amyloid, a key ingredient in Alzheimer's neuropathology".

"HSV wasn't one of the ones we found in the sequencing of the brain. In those patients, viral proteins were discovered in the spinal fluid of some Lou Gehrig's patients, and patients with positive viral protein tests in their spinal fluid showed benefit when treated with antiviral drugs". Using techniques in bioinformatics, the study integrates high-throughput data into probabilistic networks that are postulated to account for the associations between herpesviruses and the telltale effects of AD. "But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology".

The research is undoubtedly compelling, but not everyone in the scientific community is convinced it means much.

"The integrated findings of this study suggest that AD biology is impacted by a complex constellation of viral and host factors acting across different timescales and physiological systems", the researchers wrote. In fact, in North America it is estimated that 90 percent of children have at least one of these viruses in their blood early in life.

Doctors don't know what causes Alzheimer's disease or the best way to treat it, but they have new evidence to suggest that a common virus may play a role in who develops the condition.

The research study does not suggest that Alzheimer's disease is contagious. And the two viruses they found to be most strongly associated with Alzheimer's, HHV-6A and HHV-7, were not as abundant in the brains of those with other neurodegenerative disorders.

"When we started analyzing the differences, it just sort of came screaming out at us from the data", Dudley says. "But it would be negligent for us to ignore these results until the next study reports back, which will take several years".

"And now, not only is the viral hypothesis resurrected: it has specific testable pathways and networks and interactions that can be explored and reconciled with the rest of the work emerging in Alzheimer's".



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