Researchers at the Icahn School of Medicine in NY and Arizona State University in Tempe conducted RNA sequencing on data from 3 brain banks to evaluate differential viral abundance in AD.
Analysis of large data sets from post-mortem brain samples of people with and without Alzheimer's disease has revealed new evidence that viral species, particularly herpesviruses, may have a role in Alzheimer's disease biology. That's when they started getting odd results.
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. HHV-6A is a usually symptom-less virus that infects people later in life.
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. To probe this question, the team created the equivalent of a biological social network to probe how various molecular and genetic signals were interacting with each other.
They also found that multiple points overlapped between virus-host interactions and genes associated with Alzheimer's risk, and multiple viruses that impact Alzheimer's disease were found in DNA, RNA and proteins. "It was really striking", says Sam Gandy, a co-author who is a Mount Sinai neurologist and amyloid expert.
"This analysis allowed us to identify how the viruses are directly interacting with or coregulating known Alzheimer's genes". 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. Sure enough, the animals developed more of those amyloid plaques.
The Alzheimer's community remains cautious about the findings.
Researchers made the discovery after examining data from brain banks and cohort studies that are part of the Accelerating Medicines Partnership - Alzheimer's Disease consortium.
Viruses that sneak into the brain just might play a role in Alzheimer's, scientists reported Thursday in a provocative study that promises to re-ignite some long-debated theories about what triggers the mind-robbing disease.
Gandy and Dudley stress that they don't believe Alzheimer's is an infectious disease that can be transmitted like the common cold.
"We didn't have a horse in this virus race whatsoever", says Dudley. Something needs to activate the viruses, which causes them to begin replicating. It seems feasible that amyloid is not the cause of disease in many cases.
They found that Alzheimer's biology is likely impacted by a complex group of viral and host genetic factors.
"To be clear, it does not prove the idea that viruses causes Alzheimer's".
And like other herpes viruses, it can flare up after having been dormant for decades. According to the so-called pathogen hypothesis of AD, the brain reacts to infection by engulfing viruses with the protein amyloid beta (Aβ), sequestering the invaders and preventing them from binding with cell surfaces and inserting their viral genetic payload into healthy cells. Those efforts have failed to improve brain function even when they accomplished their immediate goal.
President to sign "something" on migrant children
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