Double Protection: Shingles Vaccine Reduces Risk and Progression of Dementia

Recent research shows that the shingles vaccine may help reduce the risk of dementia, decrease cases of mild cognitive impairment, and even reduce deaths from dementia in people who already have the disease. This is likely because the vaccine prevents reactivation of the varicella-zoster virus, which can cause inflammation in the brain, and also because it strengthens the immune system of the elderly as a whole. These effects were observed in two different countries using very reliable methods.

Science already knows that neuroinflammation, that is, inflammatory processes within the brain, plays an important role in the development and worsening of various types of dementia. This led researchers to consider whether certain viruses that can reach the nervous system could also contribute to this process.

Among these viruses, neurotropic herpesviruses are the most studied. They are noteworthy because, after the first infection, they do not go away: they remain "dormant" within the nervous system throughout life and can "wake up" again, especially with advancing age. Furthermore, they are known to cause inflammation in the brain, as in cases of encephalitis.

Some recent findings have further reinforced this hypothesis. For example, it has been observed that certain herpesviruses can promote the formation of beta-amyloid and phosphorylated tau, two proteins strongly linked to Alzheimer's disease.

There is also evidence that another virus in the family, the Epstein-Barr virus, is likely an important causal factor in multiple sclerosis. All of this has increased interest in understanding whether similar viruses could influence the onset of dementia.

The varicella-zoster virus, which causes chickenpox and, later in life, shingles, is especially relevant. Even when a person has no visible symptoms, it can silently reactivate and generate constant pressure on the immune system. This repeated reactivation can trigger inflammation in both the peripheral nervous system and within the brain, impairing the immune balance of older people.

Furthermore, the varicella-zoster virus has been associated with the formation of amyloid plaques, tau accumulation, and even vascular damage in the brain, similar to that observed in many cases of dementia.

Given this, the idea that vaccination against shingles could help makes sense. If the vaccine reduces these viral reactivations, it could decrease some of this chronic inflammation affecting the brain. This could not only reduce the risk of dementia but also preserve immune health and even help maintain cognitive ability in older adults.

Furthermore, recent studies suggest that some vaccines may offer indirect health benefits, meaning positive effects beyond protection against the target microorganism. They can modulate the immune system more broadly and reduce so-called "immunosenescence," which is the natural weakening of the immune system with age.

Interestingly, these extra effects tend to be stronger in women and also occur more prominently in vaccines made with live attenuated viruses, as is the case with the shingles vaccine analyzed in this study.

One of the most important elements of this line of research is a near-natural randomization that occurred in Wales. The British National Health Service implemented the shingles vaccine with strict eligibility rules based solely on the day of birth.

As a consequence, people who had their birthday in a specific week had almost a 50% greater chance of receiving the vaccine than people born just a few days earlier. This created a situation similar to a controlled experiment: two groups almost identical in everything—health, lifestyle, socioeconomic profile—but differing mainly in the likelihood of having been vaccinated.

Thus, it was possible to compare the incidence of dementia between these groups without the concern that "healthier" people would automatically be the ones who choose to get vaccinated, something that often distorts traditional observational studies.

When researchers analyzed these groups over seven years, they found that vaccination prevented approximately one in five new cases of dementia. Later, using an identical scenario in Australia, they found virtually the same result, reinforcing that the effect was not specific to a single population.

Although these previous studies had clearly shown that the vaccine appeared to reduce new cases of dementia, it was still unclear at what point in the disease process this benefit occurred. Does the vaccine only help before dementia develops? Or can it also help people who already have a diagnosis?

To answer this, the new study focused on two extreme points of the disease: on the one hand, observing whether vaccination reduces new diagnoses of mild cognitive impairment (MCI), which is often the first clinical sign of dementia; on the other hand, assessing whether the vaccine reduces deaths from dementia among those who already have the disease.

The methodology followed the same principle of “quasi-randomization” based on birth date, because this ensures that comparisons are fair, reducing the chance of external factors influencing the results. Since there were no large-scale population-based amyloid or tau tests during the study period, the researchers used these two extreme clinical markers (mild cognitive impairment and death from dementia) to map the possible impact of the vaccine throughout the entire disease trajectory.

The results showed a beneficial effect at both points: vaccination reduced both new diagnoses of mild cognitive impairment and deaths from dementia among people already diagnosed.

This indicates that the vaccine appears to act at all stages of the clinical course of dementia, preventing its onset and also slowing its progression. The data also suggest that these effects are not specific to a particular type of dementia, reinforcing the hypothesis that the main mechanism may be immunological and not related to a single pathogen.

Thus, this set of studies suggests that vaccination against herpes zoster with live attenuated virus may play an important role in cognitive protection throughout old age, offering benefits that go beyond the prevention of herpes zoster itself and possibly influencing brain health in a broader sense.

LEIA MAIS:

The effect of shingles vaccination at different stages of the dementia disease course

Min Xie, Markus Eyting, Christian Bommer, Haroon Ahmed, and Pascal Geldsetzer

Cell. 2 December 2025

DOI: 10.1016/j.cell.2025.11.007

Abstract:

Using natural experiments, we have previously reported that live-attenuated herpes zoster (HZ) vaccination appears to have prevented or delayed dementia diagnoses in both Wales and Australia. Here, we find that HZ vaccination also reduces mild cognitive impairment diagnoses and, among patients living with dementia, deaths due to dementia. Exploratory analyses suggest that the effects are not driven by a specific dementia type. Our approach takes advantage of the fact that individuals who had their eightieth birthday just after the start date of the HZ vaccination program in Wales were eligible for the vaccine for 1 year, whereas those who had their eightieth birthday just before were ineligible and remained ineligible for life. The key strength of our natural experiments is that these comparison groups should be similar in all characteristics except for a minute difference in age. Our findings suggest that live-attenuated HZ vaccination prevents or delays mild cognitive impairment and dementia and slows the disease course among those already living with dementia.