It can occasionally be brought on by stress, disease, or trauma, which causes cold sores in certain people. However, the same virus, known as herpes simplex virus type 1, may also be a major contributor to Alzheimer’s disease, which is much more deadly.

My coworkers and I made an unexpected finding more than 30 years ago. We discovered that older adults may have this cold sore virus in their brains. It was the first obvious indication that a virus might be stealthily residing in the brain, which was long believed to be germ-free due to the so-called “blood-brain barrier.”

Then we found something much more remarkable. Individuals who have been infected with this virus and have a certain gene (APOE-e4) that raises their risk of Alzheimer’s disease are at a significantly higher risk.

We examined brain cells that we infected with the virus in order to conduct additional research. They generated the same aberrant tau and amyloid proteins that are present in Alzheimer’s patients’ brains.

We think that for years, if not decades, the virus remains mostly dormant in the body. However, when the immune system deteriorates with age, it may reawaken in the brain. When it does, inflammation and brain cell damage will result. In certain people, recurrent flare-ups may eventually result in the kind of damage that causes Alzheimer’s.

Later, we discovered that the sticky clusters of these proteins, which are present in Alzheimer’s patients’ brains, contain the virus’s DNA. More promisingly, antiviral therapies decreased this damage in the laboratory, indicating that medications may eventually aid in delaying or perhaps preventing the illness.

Others’ large population studies revealed that certain antiviral treatments decreased the incidence of Alzheimer’s and that severe infections, particularly those caused by the cold sore virus, were a powerful predictor of the disease.

We continued our investigation after that. We pondered whether other viruses, such the one that causes shingles and chickenpox, would have comparable effects when dormant in the body.

Shingles vaccine offers another clue

We discovered something intriguing when we examined the medical records of hundreds of thousands of patients in the United Kingdom. Patients with shingles only marginally increased their risk of dementia. However, the risk of developing dementia was lower for those who had the shingles vaccine.

Similar findings were found in a recent study done by Stanford University.

This confirmed our long-held hypothesis that lowering the risk of Alzheimer’s disease might be achieved by preventing frequent illnesses. Other trials consistently demonstrated that infections were a risk factor and that certain other vaccines provided protection against Alzheimer’s.

Next, we looked into how the hidden virus in the brain might be activated by Alzheimer’s risk factors such infections and head trauma.

We discovered that the cold sore virus reactivated and caused damage akin to that observed in Alzheimer’s disease when we added other infections or simulated a brain injury using a sophisticated 3D model of the brain with a dormant herpes infection. However, the virus remained dormant and the damage was prevented when we used a therapy to lessen inflammation.

All of this points to the possibility that the virus that causes cold sores may have a significant role in Alzheimer’s disease, particularly in those who have specific genetic risk factors. Additionally, it makes room for potential novel approaches to disease prevention, such vaccinations or antiviral medications that prevent the virus from awakening and damaging the brain.

What started out as a connection between memory loss and cold sores has developed into a much larger story that could someday help us comprehend and lower the danger of one of the most dreaded illnesses of our time.

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