
The cold-sore virus many people catch in childhood often stays in the body for life, lying dormant in the nerves. That virus, herpes simplex virus type 1 (HSV-1), may play a role in the development of Alzheimer’s disease.
That finding comes from Ruth Itzhaki, an honorary professor of molecular neurobiology at the University of Manchester and a visiting research fellow at the University of Oxford.
More than 30 years ago, Professor Itzhaki’s team made a striking discovery: they found HSV-1 in the brains of older adults.
For the first time, scientists learned the virus could quietly reside in the brain — long thought to be microbe-free and protected by the blood–brain barrier.
What else have scientists discovered?
Itzhaki and her colleagues then uncovered something even more astonishing. People who carried a particular version of the APOE-ε4 gene and who were infected with HSV-1 had a markedly higher risk of developing Alzheimer’s.
In brain cells infected with the virus, the team observed production of the same abnormal proteins — amyloid and tau — that appear in Alzheimer’s brains.
Researchers believe the virus can remain dormant for many years. When the immune system weakens, the virus can cross into the brain and reactivate. When that happens, it damages brain cells and triggers inflammation, as reported by ScienceAlert.
Over time, repeated flare-ups can produce the gradual damage that leads to Alzheimer’s disease.
Itzhaki says other teams have also found that severe infections, particularly those caused by herpes viruses, are strong predictors of Alzheimer’s. She argues that targeted antiviral treatment could reduce that risk.
What about other dormant viruses?
Itzhaki’s team didn’t stop there. The scientists investigated whether other dormant viruses in the body — such as varicella-zoster virus, which causes chickenpox and shingles — could have similar effects.
By examining medical records from hundreds of thousands of Britons, the researchers found that people who had shingles faced a slightly higher risk of dementia, while those who received the shingles vaccine had a lower risk.
That supports the idea that preventing common infections could lower the risk of Alzheimer’s disease.
In summary, Professor Ruth Itzhaki says herpes could be an important contributor to Alzheimer’s, especially in people with certain genetic risk factors. Her team’s findings open the door to developing preventive measures that could keep the virus from reactivating and damaging the brain.