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This Common Virus May Be Quietly Raising Your Alzheimer’s Risk

May 24, 2025 at 7:13:27 PM

HSV-1 and Alzheimer’s Disease: New Research Suggests Antivirals May Offer Protection

New research is uncovering a surprising connection between HSV-1 and Alzheimer’s disease. Herpes simplex virus type 1 (HSV-1), the virus best known for causing cold sores, may play a hidden role in increasing the risk of Alzheimer’s. A large study analyzing health data from hundreds of thousands of patients found that people infected with HSV-1 were 80% more likely to develop Alzheimer’s disease compared to those without the infection.


This doesn't mean HSV-1 causes Alzheimer's directly, but the association is significant enough that it’s raising important questions for public health and future treatment strategies.


A Closer Look at the Research

Researchers used data from over 340,000 individuals to compare those with Alzheimer’s to those without neurological conditions. They discovered that people with HSV-1 were more commonly diagnosed with Alzheimer’s—even after accounting for age, sex, health visits, and other risk factors.

Here’s what they found:

  • People with HSV-1 were 80% more likely to have Alzheimer’s.

  • Those who took antiviral medications like acyclovir or valacyclovir were 17% less likely to develop Alzheimer’s than HSV-1 patients who didn’t take these drugs.

The protective effect of antivirals suggests that inflammation or viral activity in the brain may influence the development of neurodegenerative diseases.



How Could HSV-1 Impact Brain Health?

HSV-1 is a neurotropic virus, meaning it can infect the nervous system. Scientists believe that HSV-1 might contribute to Alzheimer’s by:

  • Triggering chronic brain inflammation

  • Increasing amyloid-beta plaque buildup, a key feature of Alzheimer’s

  • Activating the brain’s immune response in harmful ways

Interestingly, the virus’s DNA has even been found in the brain plaques of Alzheimer’s patients. The connection may be especially strong in individuals who carry a genetic risk factor for Alzheimer’s called ApoE ε4, which also makes them more vulnerable to HSV-1 infection.



Antiviral Therapy and Alzheimer’s Prevention

Could antivirals reduce dementia risk?

While this was an observational study—meaning it doesn’t prove cause and effect—it adds to growing evidence that managing HSV-1 could reduce the risk of Alzheimer’s disease. People who took antiviral medications for HSV-1 were significantly less likely to develop Alzheimer’s, pointing to a possible preventive strategy.

More research is needed, but these findings support the idea that common viruses could play a larger role in brain aging than previously thought.



Why This Matters for Public Health

Alzheimer’s currently affects over 35 million people worldwide. With no cure available, prevention is essential. If viruses like HSV-1 contribute to the disease process, improving virus prevention, early detection, and access to antiviral treatments could become vital tools in lowering dementia rates globally.


Conclusion

The link between HSV-1 and Alzheimer’s disease is gaining attention. While more research is necessary, this study suggests that controlling herpes virus infections may be a promising direction in the fight against dementia. It’s a reminder that sometimes, preventing a common infection might have profound effects on long-term brain health.

Discover more at https://www.interventionalpsychiatry.org/


Citations:

  1. Lopatko Lindman, K., et al. (2024). Association Between Herpes Simplex Virus Type 1 and Alzheimer's Disease: A Case-Control Study. BMJ Open. https://bmjopen.bmj.com

  2. Itzhaki, R.F. (2020). Herpes Simplex Virus Type 1 and Alzheimer’s Disease: Increasing Evidence for a Major Role of the Virus. Frontiers in Aging Neuroscience. https://www.frontiersin.org/articles/10.3389/fnagi.2020.00004/full

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Editorial Disclaimer:

This article was produced using a combination of editorial tools, including AI, as part of our content development process. All content is reviewed by human editors before publication.

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