A picture of a doctor drawing out the vaccine with a syringe whilst wearing gloves on both hands

The shingles vaccine could slow the progression of dementia, according to a new study led by Stanford University in the US.

Researchers revealed in April that older adults who had received the shingles vaccine were 20% less likely to develop dementia within seven years.

A follow-up study, published on December 2 in Cell, found that the vaccine may also benefit those already diagnosed with dementia by slowing the progress of the disease.

The researchers looked at the health records of more than 280,000 adults living in Wales and aged between 71 and 88 years old. They were aiming to understand the effects of a shingles vaccination programme that began in 2013.

By 2020, one in eight older adults, who were by then 86 and 87, had been diagnosed with dementia. But those who received the shingles vaccine were 20% less likely to develop dementia than the unvaccinated.

“It was a really striking finding,” said Pascal Geldsetzer, assistant professor of medicine and senior author of the study. “This huge protective signal was there, any which way you looked at the data.”

When the researchers analysed the health records further, they found that people who received the vaccine were less likely to be diagnosed with mild cognitive impairment during a nine-year follow-up than those who were unvaccinated.

What’s more, people who received the vaccine after a dementia diagnosis were significantly less likely to die from dementia in the next nine years, suggesting that the vaccine could slow the progress of the disease.

Overall, nearly half of the 7,049 Welsh seniors who had dementia at the start of the vaccination programme died from dementia during follow-up, but only about 30% of those who received the vaccine died from dementia.

“The most exciting part is that this really suggests the shingles vaccine doesn’t have only preventive, delaying benefits for dementia, but also therapeutic potential for those who already have dementia,” Geldsetzer said.

Whether the vaccine protects against dementia by revving up the immune system overall, by specifically reducing reactivations of the virus or by some other mechanism is still unknown.

Also unknown is whether a newer version of the vaccine, which contains only certain proteins from the virus and is more effective at preventing shingles, may have a similar or even greater impact on dementia.

Geldsetzer hopes the new findings will inspire more funding for this line of research.

“At least investing a subset of our resources into investigating these pathways could lead to breakthroughs in terms of treatment and prevention,” he said.

In the past two years, his team has replicated the Wales findings in health records from other countries, including England, Australia, New Zealand and Canada, that had similar rollouts of the vaccine. “We just keep seeing this strong protective signal for dementia in dataset after dataset,” Geldsetzer said.

The study author has now set his sights on a large, randomized controlled trial, which he says would provide the strongest proof of cause and effect. Participants would be randomly assigned to receive the live-attenuated vaccine or a placebo shot.

“It would be a very simple, pragmatic trial because we have a one-off intervention that we know is safe,” he said.