The virus behind the common cold sore—herpes simplex virus type 1 (HSV-1)—is typically caught in childhood and lingers silently in the body for life, hiding deep within the nerves. Occasionally, it reactivates due to stress, illness, or trauma, leading to the familiar painful blisters. But according to decades of emerging research, this seemingly harmless virus could be doing something far more sinister: contributing to the development of Alzheimer’s disease.
Over 30 years ago, my colleagues and I made a startling discovery. We found that HSV-1 was present in the brains of older adults—challenging the long-held belief that the brain is protected from infections by the so-called blood-brain barrier. It was the first compelling sign that viruses could lie dormant in the brain, unseen and underestimated.
What we discovered next was even more alarming. People who carry a common genetic risk factor for Alzheimer’s—the APOE-e4 gene—and also harbor HSV-1 in their system are at a markedly higher risk of developing the disease.
To dig deeper, we infected brain cells in the lab with HSV-1. The result? The cells began producing the same abnormal tau and amyloid proteins that accumulate in the brains of Alzheimer’s patients.
Our theory: HSV-1 lies dormant in the brain for years, even decades. But as we age and our immune system weakens, the virus can reactivate. This reawakening sparks inflammation and brain cell damage—and for some individuals, repeated flare-ups could ultimately trigger the onset of Alzheimer’s.
In a striking revelation, we later found that the sticky clumps of tau and amyloid proteins—hallmarks of Alzheimer’s disease—not only existed in infected brain tissue, but contained fragments of herpes virus DNA. This pointed to a deeper, more direct link between herpes simplex virus type 1 (HSV-1) and the development of the disease.
Even more encouraging, when we treated infected brain cells in the lab with antiviral medications, the damage was significantly reduced. These findings suggest that antiviral therapy might one day help delay—or even prevent—the onset of Alzheimer’s.
This theory gained further traction as population studies began to echo our lab results. Some large-scale studies showed that people treated with antivirals had a lower risk of Alzheimer’s, while those with frequent or severe viral infections—especially from HSV-1—faced a markedly higher risk of developing the disease.
Curious about whether other latent viruses might play a similar role, we expanded our research to include varicella-zoster virus—the culprit behind chickenpox and shingles.
A Vaccine with Unexpected Benefits
While analyzing medical records of hundreds of thousands of patients in the UK, we made an intriguing discovery. Individuals who had shingles showed only a slight increase in dementia risk. But those who received the shingles vaccine actually had a significantly reduced risk of developing dementia.
Our findings were soon backed by Stanford University, whose independent research mirrored our results. This reinforced our long-standing hypothesis: Preventing common viral infections could reduce the risk of Alzheimer’s disease. Other studies, too, found that certain vaccines—not just against shingles, but also against influenza and pneumonia—appeared to offer protective effects against Alzheimer’s.
What Triggers the Virus in the Brain?
We then turned our attention to a critical question: What causes dormant viruses in the brain to suddenly reactivate?
To find out, we used a cutting-edge 3D brain model containing latent HSV-1. When we introduced factors like inflammation, secondary infections, or brain trauma—all known Alzheimer’s risk factors—the dormant virus awoke, unleashing damage similar to that seen in Alzheimer’s patients.
However, when we treated the model with anti-inflammatory drugs, the virus remained inactive, and no damage occurred.
A New Direction in Alzheimer’s Research
Taken together, these discoveries offer compelling evidence that HSV-1 may play a significant role in Alzheimer’s disease, particularly in individuals with specific genetic vulnerabilities like the APOE-e4 gene.
More importantly, they open the door to new strategies for prevention—from vaccines and antiviral medications to therapies that target brain inflammation and viral reactivation.
What began as a surprising link between cold sores and memory loss has grown into a revolutionary new understanding of Alzheimer’s disease. It brings hope that, in the not-so-distant future, we may be able to protect the brain by targeting viruses that have been hiding in plain sight all along.