Most people think of shingles as a rash. A bad one, sure — blistering, painful, the kind of thing that ruins a few weeks of your life and then goes away. Maybe you know someone who had it across their ribs, or down one side of their face, and they told you it was excruciating. You believed them. And then you forgot about it.
That forgetting is the problem.
Because shingles, it turns out, doesn’t just hurt. It ages you. And the virus behind it — varicella-zoster, the same one that gave you chickenpox when you were seven — may be quietly doing damage to your brain for years before anyone thinks to look.
In 2010, a 63-year-old university lecturer in Colorado, a viral immunologist, began losing his ability to concentrate. His memory faltered, his reading suffered, and he couldn’t get through a lecture without pausing mid-sentence. Brain biopsies came back inconclusive. For four years, he got worse. Then he heard about a case of brain inflammation linked to varicella-zoster reactivation, remembered he’d had a brief bout of shingles before it all started, got tested, and began a course of the antiviral acyclovir. His cognition came back. Just like that.
That case, published in 2016, cracked open a door that researchers are now walking through at speed.
Here’s what we know. The varicella-zoster virus infects roughly 95 per cent of people before they’re twenty, usually as chickenpox. After you recover, the virus doesn’t leave. It retreats into your peripheral nervous system — the neurons linking brain and spinal cord to the rest of you — and stays there. Dormant. Waiting. About 30 per cent of unvaccinated people will develop shingles in their lifetime, but the visible rash is only part of the story. Saliva, blood and cerebrospinal fluid samples indicate frequent subclinical reactivation of varicella-zoster, even in healthy individuals — the virus waking up and doing its work without you ever knowing it happened.
And what does that work look like?
Bad. Really bad. Researchers at the University of Colorado Anschutz have found that shingles triggers prothrombotic exosomes — tiny lipid vesicles that carry pathogenic cargo, causing blood clotting and inflammation far from the original infection site. That mechanism, detailed in the Journal of Infectious Diseases, helps explain why shingles patients are nearly twice as likely to have a stroke within 30 days of infection. The rash clears. You feel fine. But you’re walking around with a significantly elevated stroke risk that can persist for a year or more. A Harvard-led analysis published in the Journal of the American Heart Association tracked over 200,000 adults and found the elevated stroke risk persists for 12 years or longer after a shingles episode.
Andrew Bubak, assistant professor of neurology at Colorado Anschutz, has been studying this for years. He points to varicella-zoster’s particular talent for infecting the cerebral arteries — the blood vessels that supply the brain — triggering chronic inflammation that narrows those vessels over time. That’s not just a stroke pathway. It’s a dementia pathway.
And it might be worse than that. Researchers at Tufts University, led by Dana Cairns, built 3D brain tissue models to study what happens when varicella-zoster meets another virus most of us carry: herpes simplex virus type 1, or HSV-1. When neurons already harbouring dormant HSV-1 were exposed to varicella-zoster, it triggered a reactivation of HSV-1, producing dramatic increases in tau and amyloid beta proteins — the signature markers of Alzheimer’s disease. Cairns called it a one-two punch. Two common, usually harmless viruses, together, might be setting Alzheimer’s in motion.
So. What do we do about it?
The answer, increasingly, looks like vaccination. And the data coming in is extraordinary.
A major study led by Stanford Medicine, published in Nature in April 2025, exploited a natural experiment created by Wales’s shingles vaccination programme. When Wales rolled out the vaccine in 2013, limited supply meant that adults who turned 79 just after the programme started were eligible, while those who turned 80 just before it were not. Same population. Same health behaviours. Same socioeconomic profile. The only difference was whether they got the jab. Those who received the shingles vaccine were 20 per cent less likely to develop dementia over the following seven years.
Twenty per cent. For most people, a vaccine is associated with avoiding a rash.
A follow-up study by the same team, published in Cell in December 2025, went further — finding that vaccination also reduced diagnoses of mild cognitive impairment and, among people already living with dementia, significantly lowered the likelihood of dying from it. Pascal Geldsetzer, the Stanford researcher leading the work, was blunt about the implications: the vaccine appears to have both preventive and therapeutic potential. Harvard epidemiologist Alberto Ascherio, commenting on the findings, called them “promising” and noted that the vaccine wasn’t even designed to prevent dementia, making the result, in his words, a “lucky break.”
Then, in January 2026, another piece fell into place. A study from USC’s Leonard Davis School of Gerontology, published in the Journals of Gerontology, examined over 3,800 Americans aged 70 and older and found that those who’d received the shingles vaccine showed slower biological ageing across multiple measures — lower inflammation, slower epigenetic ageing, and slower transcriptomic ageing. Not marginal differences. The benefits appeared to persist for four or more years after vaccination.
The proposed mechanism is a concept called “inflammaging” — the chronic, low-grade inflammation that accumulates in the body over decades and drives heart disease, frailty, and cognitive decline. The shingles vaccine, by keeping varicella-zoster dormant and preventing those silent reactivations, may be turning down the dial on that background fire.
There are gaps in the picture, obviously. Most of these are observational studies. Correlation and causation remain tangled in places. Nobody’s run a large randomised trial specifically testing whether the shingles vaccine prevents dementia — though the Welsh data comes about as close to a natural experiment as epidemiology gets.
But the direction of travel is clear enough that it’s changing how people think about the vaccine’s role. England launched its first routine childhood chickenpox vaccination programme in January 2026, joining the US (which started in 1995), Canada, Australia and Germany. Children who never acquire wild varicella-zoster in the first place may never face the downstream risks — the strokes, the vascular damage, the cognitive erosion decades later.
For adults, the shingles vaccine — Shingrix, a two-dose regimen — is currently recommended for those aged 50 and older. Bubak thinks that’s too late. He’s argued for offering it earlier, potentially with multiple boosters, and for developing rapid saliva tests that could detect varicella-zoster reactivation during periods of high stress. The virus responds well to antivirals, he says. Safe drugs. Cheap drugs. The problem is that most GPs don’t even think to check.
I keep coming back to that lecturer in Colorado. Four years of decline. Four years of tests that missed it. And then a course of antivirals, and his mind came back. How many people are out there right now, experiencing what looks like normal ageing — the forgetting, the fog, the slowing down — when what’s actually happening is a virus they caught at age five is eating into their cerebral vasculature?
We don’t know. That’s the honest answer. But we’re getting closer to finding out, and the tools to address it already exist. They’re sitting in pharmacy fridges. Two jabs, two to six months apart.
It’s not the whole answer to dementia. Nothing is. But if even a fraction of the emerging data holds up, it might be one of the cheapest, simplest interventions we’ve ever had against cognitive decline.
And right now, most people still think shingles is just a rash.
The Virus You Forgot About May Be Ageing Your Brain was originally published in BeingWell on Medium, where people are continuing the conversation by highlighting and responding to this story.
