A Colorado lecturer's unexplained cognitive decline was ultimately linked to a reactivation of the varicella-zoster virus (which causes chickenpox and shingles). His symptoms reversed after antiviral treatment, highlighting a previously underestimated connection between the virus and brain health.
Emerging research, including a major 2025 study, suggests the shingles vaccine may prevent a significant portion of dementia cases and slow biological aging. This is attributed both to avoiding the direct neurological damage from viral reactivation and to broader immune benefits.
The findings underscore the importance of vaccination, both in childhood against chickenpox and in adulthood against shingles, to prevent the virus from reactivating and potentially harming cognitive function later in life.
Main topics: Varicella-zoster virus reactivation, cognitive decline/dementia, shingles vaccine, brain health, vaccination benefits.
In 2010, a university lecturer from Colorado started experiencing worrying signs of cognitive decline.
The lecturer—a 63-year-old viral immunologist whose identity has been kept anonymous—suffered alarming symptoms, including impaired memory, waning concentration, and difficulty reading. While giving lectures to students, he found he had difficulty focusing and was often unable to finish sentences without pausing. But medical tests, including a brain biopsy, failed to get to the source of the problem, and over the next four years, his symptoms continued to progress.
His decline would have likely continued unabated had he not heard about a case of encephalitis—serious brain inflammation caused by a reactivation of the varicella-zoster virus, most commonly associated with childhood chickenpox and, later in life, shingles.
Remembering that his own symptoms had been preceded by a brief case of shingles, subsequent tests confirmed the patient had indeed experienced a reactivation of varicella-zoster. And so he decided to treat the problem with a course of acyclovir, an antiviral drug commonly prescribed to shingles patients. To his colleagues’ amazement, the Colorado lecturer’s symptoms quickly faded away and his cognition returned to normal.
This remarkable case study, published in 2016, has inspired neurovirologists to look deeper into the connection between shingles and brain aging. For decades, shingles has been predominantly associated with a form of nerve pain known as postherpetic neuralgia, which can be so severe that it was once cited as the leading cause of pain-related suicide in the elderly. Now, research is starting to reveal the devastating impact that shingles can have on brain health.
According to Andrew Bubak, assistant professor of neurology at the University of Colorado Anschutz, the true burden of varicella-zoster “is totally underestimated. But it’s a very treatable virus.”
In recent years, increasing numbers of studies have shown that the shingles vaccine appears to be capable of protecting the aging body and brain, and dementia specialists are taking note. In April 2025, a major study by researchers at Stanford University suggested vaccination against shingles could prevent one in five new cases of dementia. More recent studies have also linked getting a shingles vaccine to slower biological aging across a variety of measures.
One explanation given for the findings is that the vaccine might be stimulating the immune system in a broadly beneficial manner. While there is likely some truth in this, additional research increasingly points to the value of avoiding shingles (or reactivations of the varicella-zoster virus) in the first place, with two separate studies finding associations between shingles and self-reported cognitive decline and dementia.
Neurovirologists believe this emerging data underlines the importance of avoiding infection, through the childhood chickenpox vaccination—given to children in the US since 1995 and introduced in the UK in January 2026—and through the adult shingles vaccine and booster jabs in later life.
Before the US started routinely vaccinating against chickenpox, more than 90 percent of children acquired the varicella-zoster virus in childhood. Following the infection, the virus takes up position in the peripheral nervous system—the neurons linking the brain and spinal cord to the limbs and organs—where it stays dormant, sometimes for decades.
Varicella-zoster can reactivate in the body following various triggers, which range from acute stress to concussion, co-infections with Covid-19, immunosuppressive medications, and the general aging of the immune system. In many cases, such reactivations may be completely symptomless, with some studies suggesting many of us could unknowingly experience repeated “subclinical” reactivations—the virus reawakening from its dormant state without inducing visible symptoms—in mid- to later life.
“We rely on specialized immune cells to continuously patrol the nervous system and keep the dormant virus suppressed,” says Tian-Shin Yeh, associate professor of medicine at Taipei Medical University and attending physician at Shuang Ho Hospital in Taiwan. “As we get older, these cells can become less effective, or exhausted.”
Once varicella-zoster reactivates, several things can take place. The virus is part of the herpes family, members of which are particularly adept at infiltrating the brain and central nervous system due to their ability to exploit its internal transport mechanisms for their own use. “Our nerve cells contain molecular motors that shuttle cargo along the nerve fibers,” says Yeh. “Herpes viruses can commandeer these transport systems to move from peripheral tissues deep into the nervous system.”
Like other herpes viruses, researchers believe that varicella-zoster can damage DNA and mitochondria within the brain’s neurons, accelerating the biological aging process. Evidence suggests the virus also has a particularly unique ability to infect the cerebral arteries that supply and perfuse the brain, driving a chronic inflammatory response which causes the narrowing of these blood vessels.
Bubak believes that this is one of the reasons why having shingles greatly increases your likelihood of a stroke—studies warn of an 80 percent higher risk of stroke in the first month following shingles, with the risk remaining 20 percent higher a year later. Bubak also says that it’s a likely explanation for the link between varicella-zoster reactivation and vascular dementia. “It’s a significant accelerator,” he says, “the evidence supports that it’s causing inflammation of the cerebral vasculature, which is driving cognitive impairment in the elderly.”
There may also be secondary ways in which varicella-zoster can harm the brain. Epidemiological studies have long suggested a correlation between reactivation of another herpes virus, which we acquire in childhood and which stays dormant in the body—herpes simplex virus (HSV-1)—and Alzheimer’s disease. Research suggests that varicella reactivation can also trigger HSV-1 to reactivate, potentially bombarding the brain with two herpes viruses at once.
“What the shingles vaccine is really doing is possibly preventing varicella reactivation, but perhaps more importantly HSV-1 reactivation,” explains Dana Cairns, a researcher at Tufts University.
So what can we do? Cairns and colleagues point to the potential role of antioxidant supplements such as resveratrol and epigallocatechin gallate—found in green tea—as a way of mitigating some of the damage done to the brain by varicella reactivation and other herpes viruses.
However, given emerging data on the prevalence of reactivations, Bubak believes there’s a strong case for offering the shingles vaccine to people much earlier in life—it is currently recommended for adults over 50—potentially followed by multiple boosters to ensure the virus stays dormant. His research has convinced him that accelerated brain aging could also be avoided through commercializing rapid saliva tests for varicella-zoster, tests people could take during times of high stress to assess whether the virus has reactivated in their bodies. “The virus is very responsive to antivirals,” he says. “And they’re safe drugs.”
But perhaps most crucially of all, the emerging data indicate that childhood vaccination programs for chickenpox, which ensure that recipients are only ever infected with a weakened version of varicella-zoster, could reduce rates of certain dementias in decades to come.
Like Bubak, Andrew Pollard, professor of infection and immunity at the University of Oxford, believes further investigation is needed to understand the ideal time frame for shingles vaccination, including potentially offering the vaccines earlier in life. “These fascinating findings might lead to an increased possibility for more of us enjoying a healthy old age with less cognitive decline and lower burden on beleaguered health and social care systems,” says Pollard. “With the numbers of people over 65 years of age set to double this century, anything that helps reduce rates of neurological decline matters a lot.”
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