Shingles virus linked to dementia risk, research suggests
Scientists say vaccination and antiviral treatments could protect cognitive health later in life
A puzzling medical case involving a Colorado university lecturer more than a decade ago is helping reshape scientists’ understanding of how a common virus linked to chickenpox and shingles may influence brain aging—and possibly dementia.
In 2010, a 63-year-old viral immunologist began experiencing troubling neurological symptoms. The respected lecturer noticed his memory worsening, his ability to concentrate slipping, and his reading comprehension declining. During lectures, he struggled to maintain his train of thought and sometimes could not complete sentences without long pauses, according to an article in Wired.
For years, doctors searched for answers. Extensive medical testing—including a brain biopsy—failed to identify the cause. As the symptoms gradually worsened over four years, the case seemed to defy explanation.
Then a clue emerged.
The scientist recalled that shortly before his cognitive problems began, he had experienced a brief bout of shingles, a painful rash caused by reactivation of the varicella-zoster virus—the same virus responsible for childhood chickenpox.
Doctors ordered additional tests, which confirmed that the virus had indeed reactivated in his body. The lecturer then began treatment with acyclovir, an antiviral medication commonly prescribed for shingles.
The result was dramatic. According to a case study published in 2016, his symptoms rapidly improved and his cognitive function returned to normal.
The remarkable turnaround has since sparked growing interest among neurologists and virologists in the possibility that shingles and related viral activity could play a significant role in brain aging and cognitive decline.
A Hidden Burden
For decades, shingles has primarily been associated with a debilitating nerve condition known as postherpetic neuralgia, which causes severe chronic pain after the shingles rash disappears. In the past, this condition was even cited as a leading cause of pain-related suicide among older adults.
But emerging research suggests the virus may also have profound effects on the brain itself.
“The true burden of varicella-zoster is totally underestimated,” said Andrew Bubak, an assistant professor of neurology at the University of Colorado Anschutz Medical Campus. “But it’s a very treatable virus.”
In recent years, scientists have begun uncovering evidence that preventing shingles—primarily through vaccination—may also reduce the risk of cognitive decline and dementia.
One of the most striking findings came in April 2025, when researchers at Stanford University reported that vaccination against shingles could potentially prevent roughly one in five new cases of dementia.
Other studies have linked shingles vaccination to slower biological aging across multiple health indicators.
Dormant virus, decades later
The varicella-zoster virus has an unusual life cycle that allows it to remain in the body for decades.
Before routine vaccination against chickenpox began in the United States in 1995, more than 90 percent of children contracted the virus at some point during childhood. After the infection subsides, the virus does not disappear. Instead, it hides in the nervous system.
Specifically, varicella-zoster remains dormant in the peripheral nervous system, which connects the brain and spinal cord to the rest of the body.
Under certain circumstances, the virus can reactivate.
When it does, it typically produces shingles—a painful blistering rash that most often affects older adults. But researchers now believe many reactivations may occur without obvious symptoms, a phenomenon known as “subclinical reactivation.”
Scientists suspect that people may experience these silent viral flare-ups repeatedly during midlife and older age.
Aging immune systems
One reason shingles becomes more common with age is that the immune system gradually weakens.
“We rely on specialized immune cells to continuously patrol the nervous system and keep the dormant virus suppressed,” explained Tian-Shin Yeh, an associate professor of medicine at Taipei Medical University and an attending physician at Shuang Ho Hospital in Taiwan, in the Wired story.
“As we get older, these cells can become less effective, or exhausted.”
When the virus reactivates, it can travel along nerve pathways toward the central nervous system.
Herpes-family viruses—including varicella-zoster—are particularly skilled at exploiting the body’s internal transport systems inside nerve cells.
Damage inside the brain
Once inside the nervous system, varicella-zoster may trigger several processes that harm brain cells.
Researchers believe the virus can damage both DNA and mitochondria—the energy-producing structures inside cells—accelerating the aging of neurons.
Another major concern involves the virus’s ability to infect the arteries that supply blood to the brain.
This infection can trigger chronic inflammation in the blood vessels, causing them to narrow and reducing blood flow to brain tissue.
Such vascular damage may explain why shingles significantly increases the risk of stroke.
Studies show that people who develop shingles face an 80 percent higher risk of stroke during the first month following infection. Even a year later, the risk remains about 20 percent higher than normal.
According to Bubak, this vascular inflammation could also help explain links between shingles and vascular dementia, a form of cognitive impairment caused by reduced blood flow to the brain.
“It’s a significant accelerator,” Bubak said. “The evidence supports that it’s causing inflammation of the cerebral vasculature, which is driving cognitive impairment in the elderly.”
A viral double hit
The virus may also affect the brain indirectly by interacting with other dormant viruses already present in the body.
Many people carry herpes simplex virus type 1 (HSV-1), which typically causes cold sores but can also infect the nervous system.
Epidemiological studies have long suggested a connection between HSV-1 reactivation and Alzheimer’s disease.
Researchers now believe shingles outbreaks may trigger the reactivation of HSV-1 as well—potentially exposing the brain to two viruses simultaneously.
“What the shingles vaccine is really doing is possibly preventing varicella reactivation, but perhaps more importantly HSV-1 reactivation,” said Dana Cairns, a researcher at Tufts University who studies viral links to neurodegenerative disease.
Vaccination and Prevention
The growing body of evidence is prompting renewed interest in vaccination strategies.
Currently, health authorities in the United States recommend the shingles vaccine for adults age 50 and older. The vaccine significantly reduces the risk of developing shingles and its painful complications.
But some researchers believe the vaccine may offer broader benefits by preventing viral reactivation that could harm the brain.
Childhood vaccination against chickenpox may also play a long-term role in reducing dementia risk. The vaccine uses a weakened form of the virus, which may be less likely to reactivate later in life.
The United Kingdom introduced routine chickenpox vaccination for children in January 2026, bringing its policy more in line with the United States and several other countries.
Scientists say such vaccination programs could influence dementia rates decades from now.
New Ideas for Detection
Beyond vaccination, researchers are exploring ways to detect viral reactivation early—before it causes symptoms or long-term damage.
Bubak and his colleagues are investigating the possibility of rapid saliva tests that could detect varicella-zoster reactivation.
Such tests might be used during periods of high stress, illness, or immune suppression, when viral flare-ups are more likely.
If detected early, doctors could prescribe antiviral drugs such as acyclovir to suppress the virus.
“The virus is very responsive to antivirals,” Bubak said. “And they’re safe drugs.”
Lifestyle and Nutritional Approaches
Some researchers are also examining whether dietary compounds could help protect the brain from viral damage.
Dana Cairns and her colleagues have suggested that antioxidant compounds such as resveratrol—found in grapes and red wine—and epigallocatechin gallate, a compound in green tea, may help reduce inflammation or oxidative stress triggered by viral activity.
However, scientists caution that evidence for these approaches remains preliminary.
Vaccination and antiviral treatment remain the most established methods for preventing shingles and its complications.
Rethinking vaccine timing
The emerging research is also prompting questions about whether shingles vaccination should begin earlier in life.
Bubak believes vaccination strategies may eventually evolve to include earlier immunization and periodic booster shots to maintain protection as the immune system ages.
Andrew Pollard, a professor of infection and immunity at the University of Oxford, says more research is needed to determine the optimal timing.
“These fascinating findings might lead to an increased possibility for more of us enjoying a healthy old age with less cognitive decline,” Pollard said.
He noted that the stakes are growing as global populations age rapidly.
“With the numbers of people over 65 years of age set to double this century,” he said, “anything that helps reduce rates of neurological decline matters a lot.”