Cold Sore Virus May Increase Dementia Risk

A common virus that causes cold sores may play a significant role in the development of Alzheimer’s disease and dementia, according to new research.

The herpes simplex virus 1 (HSV-1), which affects nearly two-thirds of the global population under age 50, could be more dangerous than previously thought—but antiviral treatments might help reduce the risk.

The findings come from a large U.S. study published May 20 in BMJ Open, adding to growing evidence that infections may contribute to neurological decline later in life. Researchers analyzed healthcare data from over 344,000 matched pairs of patients, making it one of the most comprehensive investigations into this connection to date.

What makes this discovery particularly concerning is how widespread HSV-1 infection is worldwide. In 2016 alone, an estimated 67% of people under 50 were infected with HSV-1, according to background information in the study protocol.

The Viral Connection to Brain Health

The study revealed that people with Alzheimer’s disease were 80% more likely to have been diagnosed with HSV-1 than those without the condition, even after researchers adjusted for other risk factors.

Could this common virus that many dismiss as merely a cosmetic nuisance actually be damaging our brains over time?

The connection makes biological sense. HSV-1 is both “neuroinvasive and neurotoxic,” meaning it can enter the brain via peripheral nerves and potentially cause damage, according to the research team’s protocol. Once in the brain, the virus may trigger inflammation that contributes to the development of Alzheimer’s disease.

“It has been reported that Aβ peptides are deposited in response to HSV infection and protect host cells by blocking viral fusion with the plasma membrane, pointing to HSV as a potential risk factor for [Alzheimer’s disease],” the researchers explain in their findings.

Hope for Prevention Through Antiviral Treatment

Perhaps the most promising aspect of the research is what it reveals about potential prevention. Among the 2,330 people with documented HSV-1 infections in the study, 40% received antiviral medication after diagnosis. This treated group showed a 17% lower risk of developing Alzheimer’s disease compared to those who didn’t receive antiviral therapy.

The researchers suggest: “While the molecular mechanisms remain to be fully elucidated, these results are indicative of a possible role for antiherpetic therapy in mitigating dementia risk.”

This potential protective effect could have enormous implications for public health strategies, especially considering the growing global burden of dementia:

• Currently, about 35.6 million people worldwide live with dementia
• Approximately 7.7 million new cases are diagnosed yearly
• Alzheimer’s disease accounts for 60-80% of all dementias
• Treatment costs reached $305 billion in the U.S. alone in 2020

Beyond Cold Sores: Other Herpes Viruses Show Similar Patterns

The research didn’t stop with HSV-1. Investigators also examined other herpes family viruses and found that both HSV-2 (genital herpes) and varicella zoster virus (which causes chickenpox and shingles) were associated with increased Alzheimer’s risk.

This pattern strengthens the case that viral infections affecting the nervous system may contribute to neurological decline years or decades later.

How Viruses Might Damage the Brain

While researchers are still working to understand the exact mechanisms, several theories have emerged. HSV-1 DNA has been found in the characteristic plaques that develop in Alzheimer’s disease. Additionally, people carrying the ApoE ε4 gene variant—the most common genetic risk factor for Alzheimer’s—seem more susceptible to HSV infections.

The brain’s own defense systems might inadvertently cause damage. The researchers note that “Aβ exhibits antimicrobial properties against various pathogens, including HSV-1.” This suggests that beta-amyloid, which forms the plaques found in Alzheimer’s patients’ brains, might initially be produced as a defense against viral infection.

What begins as protection could, over time, become part of the disease process—especially with repeated viral reactivations over decades.

The Road Ahead: More Research Needed

The researchers acknowledge important limitations in their work. Many HSV-1 infections go undiagnosed because people don’t have symptoms or don’t seek treatment. And the observational nature of the study means they cannot definitively prove cause and effect.

A systematic review protocol published separately outlines plans for a more comprehensive analysis of existing evidence, with results expected in June 2025. This review aims to examine research spanning decades to provide more definitive conclusions about the HSV-1-dementia connection.

The researchers conclude their findings “place an even greater emphasis on viewing the prevention of herpes viruses as a public health priority.” With dementia cases projected to reach 152.8 million globally by 2050, understanding all potential risk factors—and especially modifiable ones like viral infections—becomes increasingly urgent.

For the millions already living with HSV-1, these findings offer both concern and hope: while the virus may increase risk, treatment options already exist that might help protect the brain. The question now is whether routine antiviral treatment could become part of dementia prevention strategies in the future.