A shingles vaccine may do more than prevent a painful rash. It may also reduce the risk of developing dementia and could even slow progression in those already diagnosed, according to a large analysis of health records from Wales.

In a new study published in Cell, researchers examined the NHS rollout of the live shingles vaccine Zostavax, which was offered based on strict date-of-birth eligibility rules. That policy quirk created an unusually useful natural experiment – a near-perfect comparison between people born just before and just after the cutoff – allowing the team to estimate how vaccination affected cognitive outcomes over time.

The analysis drew on the Secure Anonymised Information Linkage (SAIL) databank and included health records from over 300,000 people in Wales between 2013 and 2022. The authors focused on the NHS vaccine rollout that made people eligible or ineligible based on their date of birth – in other words, whether you were born a handful of days too early or too late.

That detail matters. Traditional observational studies of vaccination are often haunted by the “healthy user” problem: people who choose vaccination may also have other advantages – better access to care, fewer comorbidities, more health-conscious habits – that can masquerade as protection. Here, eligibility was determined administratively, not behaviorally; the authors describe it as a regression discontinuity design, a causal inference approach that treats the cutoff as a quasi-random assignment.

In the paper, the authors note that a one-week difference in age across the eligibility threshold produced a large difference in vaccine uptake – nearly 50 percentage points – giving them a strong lever to estimate downstream effects.

The topline message is straightforward, if not simple: eligibility for Zostavax was associated with fewer new diagnoses of mild cognitive impairment (MCI) and fewer dementia diagnoses over follow-up.

More unusually, the association did not stop at prevention. Among those already living with dementia, being eligible for vaccination was linked to a lower likelihood of dying with dementia recorded as the cause of death – a finding that raises the possibility of a disease-modifying effect, or at least a slowing of clinical decline.

A consistent feature across analyses was a stronger apparent protective effect in women than in men – a pattern that has been observed in other research on vaccine-related immune responses.

Haroon Ahmed, MD and Clinical Reader in Epidemiology at Cardiff University’s School of Medicine, who was a member of the research team, said: “Our results suggest that the shingles vaccine could potentially prevent early memory decline and slow disease progression.”

The mechanism of action is not settled. Still, the biological plausibility is not flimsy either, and it touches several themes longevity researchers have been circling for years: immunosenescence, chronic inflammation, latent infection and vascular risk.

Varicella zoster virus, the cause of chickenpox, remains dormant in the body and can reactivate later as shingles. The authors discuss the possibility that preventing reactivation may reduce neuroinflammation, with knock-on effects on pathways linked to dementia. They also mention herpes simplex, another latent virus implicated in cognitive decline, as part of a broader hypothesis that suppressing viral reactivation could reduce inflammatory and pathological cascades in the brain.

A second line of plausibility is immune training – the idea that some vaccines do more than protect against their target pathogen and may shape immune function more broadly, potentially counteracting age-related immune decline.

Then there is the vascular story. Independent research has reported that shingles vaccination may be associated with up to an 18 percent lower risk of stroke in older adults – a reminder that the boundary between neurodegeneration and vascular damage is often porous rather than neat. If vaccination reduces strokes, microvascular injury or systemic inflammation, it could plausibly slow trajectories that feed into cognitive impairment.