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As Davangere Devanand, a neurologist at Columbia University Medical Center, combed through the reams of scientific data on Alzheimer's, he stumbled across a surprising idea - could an infection be involved in driving the disease?
"I was looking for an Alzheimer's treatment approach that had a reasonable shot of working," he says. "I found this old theory, going back 35 years, which linked herpes viruses to the disease, and there were all these indirect lines of evidence."
The further Devanand looked, the more he found. Since the mid-80s, a handful of scientists around the world had doggedly pursued the idea that either a virus or a bacterium could play a role in Alzheimer's, despite almost complete antipathy from those studying more accepted theories about the disease. Colleagues snubbed them, leading scientific journals and conferences rejected their work and funding had been threadbare, but slowly and surely, they built an increasingly compelling case.
In particular, evidence pointed towards herpes simplex virus 1 (HSV-1) - a pathogen found in 70% of the UK population, and the cause of oral herpes as a prominent suspect. Studies in the UK, France and Scandinavia suggested that people who had been infected with herpes were more likely to get Alzheimer's. When Prof Ruth Itzhaki from Oxford University's Institute of Population Ageing - who has done more than any other scientist to advance the HSV-1 theory of Alzheimer's - examined postmortem brain samples from patients, she found greater amounts of the virus's DNA than in people who had not died of the disease.
"Then there was this 2018 study from Taiwan, which was quite dramatic," says Devanand. "When people with herpes were treated with a standard antiviral drug, it decreased their risk of dementia nine-fold."
This story is from the February 24, 2023 edition of The Guardian Weekly.
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This story is from the February 24, 2023 edition of The Guardian Weekly.
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