Study details

For the study, researchers looked at nearly 300,000 electronic health records gathered randomly from people born in Wales between 1925 and 1942.

Unlike the United States, which has a lower age threshold to receive the shingles vaccine, Wales decided to disqualify anyone older than 80 based on data suggesting the vaccine wasn't as effective in those older populations. Therefore, anyone born on or after September 2, 1933, would be ineligible to ever receive the shot.

When looking at the health records, the researchers found that people who received the vaccine, called Zostavax, had a 20% lower risk of later developing dementia. The shot had no impact on a variety of other health outcomes that are common in older people, including heart disease, lung infections, and cancer.

Once the researchers started looking at other areas of the world with similar vaccine rollouts, including the United Kingdom and Australia, they found similar results.

"Wherever we look, we see this strong signal," said Pascal Geldsetzer, an epidemiologist at Stanford University and author on the study. "We're looking at a causal effect. And it's specific to dementia. There is something clearly going on here."

Could viruses increase dementia risk?

While the idea that viral infections can play a role in dementia has been around for a while, it remains controversial in the Alzheimer's field, Molteni reports.

"Like most fields there is an orthodoxy; in Alzheimer's disease it's not infectious agents," said Paul Harrison, a professor of psychiatry at Oxford University. "But I've always viewed it as very intriguing."

Curhan specifically pointed to the varicella zoster virus (VZV), the same virus that causes chickenpox. After a person has chickenpox, VZV embeds itself into the nervous system within the neurons that run along the skull, the gastrointestinal tract, and other parts of the body, Molteni reports. Years ago, doctors were told that VZV went dormant in those locations.

However, recent research has shown that instead, VZV is kept in check by a person's immune system, and as people age, those immune systems break down and VZV can flare up into an active infection, coming with inflammation, a painful rash, and a variety of other complications.

During this reactivation, VZV can invade the walls of blood vessels, including the ones that cross the brain supplying it with oxygen and nutrients. "The reason I got interested is that even though there are a number of well-known risk factors for developing shingles, for most people, we don't know why they get it when they do," Curhan said.

"There are now multiple epidemiological studies showing that VZV reactivation, manifesting as shingles, increases dementia risk," said Maria Nagel, a neurovirologist who studies VZV at the University of Colorado Anschutz Medical Campus. Nagel's team has found evidence that VZV can spur the production of amyloid proteins that turn into the neurotoxic plaques that are a hallmark of Alzheimer's.

It's still unclear what mechanisms link VZV reactivation to an increased risk of dementia and more research is needed, Molteni reports. Currently, a study funded by the National Institute on Aging is investigating whether the antiviral valacycolvir, which specifically targets herpesviruses including VZV, can slow Alzheimer's progression in patients in early stages of the disease.

The National Institute on Aging has also called on researchers to apply for funding for work investigating the mechanisms that cause neurodegeneration in Alzheimer's associated with pathogens within the central nervous system, and the Infectious Diseases Society of America is also planning to hand out a round of grants in the area next year.

"That's brought in a lot of very creative people from outside the field of dementia," Nagel said. "So I really do believe that in the next 10 years or so we're going to see huge strides in finding new mechanisms and finding new ways to try to slow things down."