By Melissa Healy

Los Angeles Times

Researchers may have found a tiny culprit — human herpes virus — in the progressive loss of memory, thinking ability and identity that comes with Alzheimer’s disease. And it could be a big deal.

In research that revives a suspicion first raised more than six decades ago, scientists have found higher levels of the common virus in the brains of people who had both behavioral symptoms and neurological evidence of Alzheimer’s at the time of their death than in the brains of deceased donors who had no signs of dementia.

The researchers’ suspicions fell upon two strains of herpes virus — herpesvirus 6A and herpesvirus 7 — that were most evident in regions of the brain affected first in Alzheimer’s disease, and in those that suffer most as the disease progresses.

Their surprise discovery emerged as researchers sorted through a vast genomic data bank in search of new ideas for treating Alzheimer’s with drugs designed for other diseases. The study’s authors pored over DNA and RNA sequencing data from 622 brains donated by people affected by Alzheimer’s and 322 brains that were free of the disease.

The data they mined is usually discarded, but was archived instead by the National Institutes of Health in a bid to accelerate the discovery of new treatments by fostering “big data” collaborations. This one brought together scientists at Arizona State University’s Banner Neurodegenerative Disease Research Center and Alzheimer’s experts at New York’s Icahn School of Medicine at Mount Sinai.

It was published Thursday in the journal Neuron.

An estimated 5.7 million Americans are living with Alzheimer’s disease in 2018, a number expected to rise to 14 million by 2050 unless some means of prevention or treatment is found.

The findings are a far cry from establishing what role the two strains of the virus might play in initiating or driving the decades-long process of cognitive loss and brain changes in Alzheimer’s, or even if they play such a causative role. But it gives researchers a new foothold in a field of research that has failed to find anything to prevent, slow or reverse Alzheimer’s inexorable march.

“It is a beautiful piece of work, but it is still an association,” said Miroslaw Mackiewicz, program director at the National Institute on Aging’s Division of Neuroscience. Still, added Mackiewicz, by providing evidence for the virus’ presence and some hints at its possible role, “you have some way to start your experiments.”

If further research uncovers a key role of herpes virus in Alzheimer’s disease, “this would generate a lot of excitement because we have vaccines” against various strains of disease-causing herpes virus, said Mackiewicz.

Dr. Sam Gandy, an Alzheimer’s disease researcher at Icahn School of Medicine and one of the paper’s authors, said that if further research confirms that herpes virus is a predictable feature of Alzheimer’s disease, anti-viral treatments already in wide use might prove to be useful.

Gandy cited research that identified high levels of retrovirus in the brains of patients with Amyotrophic Lateral Sclerosis (ALS, or Lou Gehrig’s Disease). Even as researchers are still uncertain what role such viruses play in the disease, a clinical trial is underway to explore whether treatment with an anti-retroviral therapy used to treat HIV may affect the progression of ALS.

Herpes virus may not play a direct role in Alzheimer’s disease at all, the authors of the new research acknowledge.

There are many possible explanations for why herpes virus levels were so high in brains affected by Alzheimer’s. Among them: that Alzheimer’s might be an inflammatory or immune system reaction. High levels of herpes virus might have touched off such a reaction, the authors of the new research note. Or, the abundant presence of the virus could be an unrelated consequence of a brain struggling to defend itself from a different threat altogether.

But Gandy speculated that anti-viral treatment might prove effective either way.

Even if the abundance of herpes virus “is a secondary phenomenon, if it’s contributing to progression of Alzheimer’s, then treating it still could be beneficial.” Finding and treating people with a known risk for Alzheimer’s and who have high viral loads might make a difference, said Gandy.

Heather M. Snyder, senior director of medical and scientific operations for the Alzheimer’s Association, urged caution in interpreting the new findings.

“The idea that viruses or something else could be triggering or causing changes in the brain is not new,” said Snyder. “And we know that people in general, and those over 50 in particular, have these viruses in their brains. It might be more the immune system and that it may go awry. But we don’t know that.”

The new study not only “opens that door to asking those questions,” said Snyder: It highlights a new way for such discoveries to be made.

“These findings came about because of researchers’ ability to share data, samples, funding and a large dataset,” said Snyder. “That’s where increased funding continues to be so needed.”

As research teams run down the dynamics behind associations like this one, “it’s like an onion,” said Snyder. “We’re peeling back those layers and are getting to the core” of what causes Alzheimer’s disease and how to stop it.