Could an inexpensive vaccine help stave off dementia?

Anyone who has watched a loved one descend into the fog of dementia knows the tremendous toll that neurodegenerative diseases of aging can exact.

Dementia currently afflicts over 55 million people worldwide; in the US, more than 6 million people — about 1 out of 10 of those 65 years or older — live with dementia. The economic cost of treating and the often uncompensated cost of caring for those sufferers is now more than $600 billion a year. As our population ages, that number will only grow, with one estimate projecting that the number of people with dementia will double by 2060. It is a fate that many of us will one day suffer — according to one recent study, adults over 55 have a nearly one in two chance of eventually developing dementia.

But this week delivered one of the brightest spots in an otherwise dark field. According to a study that followed more than 280,000 people in Wales, older adults who received a vaccine against shingles were 20 percent less likely to develop dementia in the seven years that followed vaccination than those who did not receive the vaccine.

This could be a big deal. There are very few, if any, treatments that can prevent or slow down dementia, beyond good lifestyle habits like getting enough sleep and exercise. The possibility that a known, inexpensive vaccine could offer real protection is enormously meaningful. We have good reason to be confident in the findings: While this study is perhaps the most prominent to show the protective effects of the shingles vaccine, other studies of the vaccine have come to similar conclusions.

Beyond the promise of preventive treatment, the new study adds further evidence to a growing body of research raising the possibility that we have been thinking about neurodegenerative diseases like dementia and Alzheimer’s all wrong. It’s possible these horrible conditions are caused by a virus — and if that’s the case, eliminating the virus could be enough to prevent or treat the diseases.

To understand why the new shingles vaccine study is such a big deal, it helps to know a little bit about how medical studies are carried out.

The gold standard for research is a randomized control trial (RCT). That’s when scientists randomly assign patients to two different groups — one that receives an experimental treatment and another that doesn’t — in order to test the effectiveness of a treatment or intervention. Such RCT trials minimize bias or other complicating factors, allowing scientists to be reasonably confident that any differences between the two groups — like the likelihood of developing a disease — are due to the treatment being studied.

In the real world, RCTs are often difficult and expensive to carry out. For one thing, you need a large sample size to be confident of your results, and the control group can’t receive the treatment being studied, which creates ethical issues.

So a lot of big medical research involves observational studies, which is a fancy term for scientists observing things happening in the real world and drawing conclusions from their research. The upside is you don’t need to go through the time and trouble of gathering a big study group and randomly dividing them in two. The downside is you’re much less certain that any observed effect is due to the variables you’re studying because you don’t control the study; you just observe it,

The new study, though, took advantage of a quirk in Welsh health policy to do something better. Beginning on September 1, 2013, anyone in Wales who was 79 became eligible to receive a free shingles vaccine. (Those who were younger than 79 would become eligible once they turned that age.) But anyone who was 80 or older was not eligible on the grounds that the vaccine is less effective for the very old.

The result was what is known as a “natural experiment.” In effect, Wales had created two groups that were essentially the same — save for the fact that one group received the shingles vaccine and one group did not.

The researchers looked at the health records of the more than 280,000 adults who were 71 to 88 years old at the start of the vaccination program and did not have dementia. They focused on a group that was just on the dividing line: those who turned 80 just before September 1, 2013, and thus were eligible for the vaccine, and those born just after that date, who weren’t. Then, they simply looked at what happened to them.

By 2020, seven years after the vaccination program began, about one in eight older adults, who by that time were 86 and 87, had developed dementia. But the group that had received the shingles vaccine were 20 percent less likely to be diagnosed with the disease. Because the researchers could find no other confounding factors that might explain the difference — like years of education or other vaccines or health conditions like diabetes — they were confident the shingles vaccine was the difference maker.

A new paradigm in dementia research?

As Paul Harrison, a professor of psychiatry at the University of Oxford who was not involved in the study, told the New York Times, the research indicates that the shingles vaccine appears to have “some of the strongest potential protective effects against dementia that we know of that are potentially usable in practice.”

But this is a vaccine originally designed to prevent shingles. Why does it also appear to help with dementia?

Scientists theorize it could be related to inflammation. Shingles, or herpes zoster, is caused by the same virus responsible for chickenpox, which lies dormant in nerve cells after an initial infection and can reawaken decades later, causing painful rashes.

That reactivation creates intense inflammation around nerve cells, and chronic inflammation is increasingly recognized as a major factor in cognitive deterioration. By preventing shingles, the vaccine could indirectly protect against the neural inflammation associated with dementia.

What about the amyloid and tau protein plaques that tend to be found in the brains of people suffering from Alzheimer’s, which have long been thought of as the primary cause of the disease? It’s possible that these may actually be the body’s response to an underlying infection. That could help explain why treatments that directly target those plaques have been largely ineffective — because they weren’t targeting the real causes.

As promising as the new research is, we’re still a long way from finding a silver bullet against Alzheimer’s and dementia. One double-blinded RCT — the gold standard of the gold standard in medicine — that is underway now is examining whether valacyclovir, an antiviral used against the virus that causes shingles, could slow cognitive decline in people with early-stage Alzheimer’s. That would be a true game changer.

A version of this story originally appeared in the Good News newsletter. Sign up here!