Nobody really knows what causes Alzheimer's disease. But with someone in the world developing dementia every three seconds, according to Alzheimer's Disease International, there's a lot of research going on to try and figure it out.
A new study from the Icahn School of Medicine at Mount Sinai, published in the journal Neuron, has reignited a controversial theory about what causes the neurodegenerative disease by studying the brains of people from three different brain banks.
The researchers found that the 622 brains from people who had signs of Alzheimer's had twice the level of herpes virus present than the 322 from people who did not.
"We didn't set out to find what we found. Not even close. We were trying to find drugs that could be repurposed to treat Alzheimer's patients, but the patterns that emerged from our data-driven analysis all pointed towards these viral biology themes."
The theory that viruses could contribute to the development of dementia arose in the 1950s. It was hypothesised that Alzheimer's was a "slow virus disease," where one or several viruses steadily degraded the neurological processes in the brain after decades of lying dormant.
In more recent years, dementia researchers have leaned towards the amyloid hypothesis – where sticky plaques made from amyloid proteins accumulate outside nerve cells, or neurons, in the brain, potentially killing or blocking them.
But a study in 2014, published in the journal Alzheimer's Research & Therapy, found that this theory might have been wrong all along. The paper examined over a decade of clinical trials of drugs that targeted amyloid plaques, and found them to have a failure rate of 99.6%.
Since then, the old viral hypothesis has had a new lease of life. And the new research did find human herpes virus DNA and RNA were both more abundant in the brains of people with Alzheimer's disease.
The two strains they found most strongly associated with the disease were HHV-6A and HHV-7, which were not as prevalent in the brains of people with different neurodegenerative disorders.
Also, the researchers were able to show how viral and human genes interacted, and that genes associated with increased Alzheimer's risk were impacted by the viral DNA.
"I don't think we can answer whether herpes viruses are a primary cause of Alzheimer's disease," said Dudley.
"But what's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology."
Another possibility is that the two theories are both at work. It might be that viruses may in some way interact with human DNA and stimulate the growth of amyloid plaques.
Researchers also found in the new study that the herpes virus was involved in networks that regulate the generation of amyloid proteins.
While the findings help potentially open the door for new therapies, nothing has fundamentally changed about how to treat Alzheimer's for now, said another of the authors Sam Gandy.
Also, HHV-6A and HHV-7 are extremely common viruses, often not having any symptoms. In fact, in North America, approximately 90 percent of children have at least one of the strains in their blood in their early lives.
"Similar to other studies in this area, while this is robust research, it could not prove that the viruses actually were responsible for the disease," said James Pickett, the head of research at Alzheimer's Society.
"It therefore doesn't change what we already know about the causes of dementia, doesn't mean that having cold sores put you at increased risk of getting it and people shouldn't be unduly worried."
There's likely to be a lot of different and complicated mechanisms at play in developing Alzheimer's, which is why it has been such a challenging disease for scientists to understand.
But the authors of the new study are hopeful that resurrecting the viral hypothesis can help them explore new avenues.
"All these Alzheimer's brains in these separate, major brain banks have previously unsuspected substantial populations of herpesvirus genomes and that deserves an explanation wherever it falls in the pathogenesis," Gandy said.
"It doesn't deserve to just be brushed away."
This article was originally published by Business Insider.
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