Further Evidence for the Role Of Herpes Virus in Triggering Alzheimer’s Onset
A team of researchers from Harvard Medical School have found further evidence that supports the notion that viruses could help cause the onset of Alzheimer’s disease; an idea that was once ridiculed by other sceptics and researchers.
The work, published in Neuron, suggests that herpes viruses can spark the cascade of events that leads to the growth of new deposits of amyloid-β plaques in the brain practically “overnight,” according to senior author Rudy Tanzi, a geneticist specialising in the brain at Massachusetts General Hospital as well as Harvard Medical School.
In Alzheimer’s patients, a protein called amyloid beta clumps together to form the plaques that are thought to slowly destroy the brain. Many scientists had long assumed that amyloid-β was nothing but waste, with no meaningful purpose. But these researchers had earlier shown that amyloid-β might actually serve as a first line of defence against fungal and bacterial infection.
Mouse models that have human-like neurones were used in the study. When the mouse models were infected with the virus, they were able to better fend off brain infection than mice without them.
“The seeding of amyloid is what causes the deposition of plaque,” Tanzi said, “and herpesviruses and other microbes can rapidly seed amyloid-β.”
The study is the second in recent weeks to support the role of viruses in Alzheimer’s disease. The study was led by researchers from the Icahn School of Medicine at Mount Sinai was also published in Neuron and found evidence that herpes viruses HHV-6A and HHV-7 are more abundantly found in the brains of people who died with Alzheimer’s. The work also suggested that genes belonging to these viruses directly interact with human genes that are linked to an increased risk of the disease.