In 2013, the Welsh government rolled out the varicella zoster vaccine to older adults. It was an expected measure but it came with a curious quirk: eligibility depended on an exact birthdate. Those born on or after September 2, 1933, were invited to receive the vaccine, while those just days older were not.
The cutoff was, to an extent, arbitrary. But it created a rare and powerful opportunity to study the effects of vaccination in real-world conditions while minimizing the usual pitfalls — such as the differences in health status or lifestyle that often separate people who choose to be vaccinated from those who don’t.
Using this design, the researchers compared health outcomes among over 280,000 older adults in Wales. They found that those eligible for the vaccine were significantly less likely to develop dementia in the following seven years. After adjusting for vaccine uptake rates, the team estimated that receiving the vaccine reduced the risk of a new dementia diagnosis by 20%.
How could the shingles vaccine prevent dementia?
Both shingles and chickenpox are caused by the same virus: varicella-zoster virus (VZV). This VZV is no ordinary virus. It can lie dormant for decades in nerve tissue after causing chickenpox, only to reactivate later in life as shingles. Some scientists have long hypothesized that reactivations — especially in the brain — might play a role in triggering or accelerating dementia.
Previous studies had suggested a correlation between shingles vaccination and lower dementia risk, but these were largely observational. This new study is different because it uses the vaccine cutoff date in Wales.
But is the vaccine preventing dementia directly — or is something else at play?
The researchers explored several possibilities. The first hypothesis was that preventing shingles simply reduced the number of doctor visits, and thus the likelihood of a dementia diagnosis. But this is not likely, the study found. The effect size was too large to be explained by changes in healthcare behavior alone.
Instead, the findings point to two possible biological mechanisms. First, by preventing the reactivation of varicella zoster virus, the vaccine might reduce inflammation and damage to blood vessels and brain cells — hallmarks of Alzheimer’s and other forms of dementia. Second, the vaccine may be exerting broader, “off-target” effects on the immune system, training it to better defend against a range of infections and inflammatory processes.
Interestingly, the protective effect appeared much stronger in women than men — a pattern seen in other vaccines as well, and one that hints at complex interactions between sex hormones, immunity, and brain aging.
A shot at prevention?
It’s stunning that after decades of intense research, this vaccine appears to be the most impactful medical intervention against dementia.
Current medications offer only modest benefits, and recent drug developments targeting amyloid plaques have been controversial and costly. In that context, a widely available vaccine that could delay or prevent some cases of dementia would be a game-changer.
The idea that viruses might play a role in dementia isn’t new, but it has gained momentum in recent years. Herpes simplex virus 1 (HSV-1), the cause of cold sores, has also been detected in the brains of Alzheimer’s patients. Animal studies show that certain viruses can cause persistent inflammation or even tau protein buildup — features common in neurodegenerative disease.
This study doesn’t settle the debate, but it strengthens the case. It also raises tantalizing questions: Could boosting immunity to certain viruses in midlife delay cognitive decline later on? Are there windows of opportunity — perhaps even years before symptoms begin — when vaccines could make the biggest difference?
Researchers hope their work will spur more investigation — and perhaps spark public health agencies to take another look at the potential of old vaccines for new purposes.
The study was published in Nature.
