A new paper provides compelling evidence that the herpes virus responsible for cold sores may also be linked to Alzheimer’s disease. The findings show that antiviral drugs drastically reduce the risk of senile dementia in patients with severe herpes infections.
The review, published in the journal Frontiers in Ageing Neuroscience, raises the tantalizing prospect of a simple, effective preventive treatment for one of humanity’s most debilitating and costliest neurological disorders.
Herpes viruses are notoriously persistent. They remain lifelong in our neurons and immune cells, reactivating and resurfacing in characteristic blisters when we’re run down by stress or illness. Most people are infected by herpes simplex virus 1 (HSV1) by the time they reach old age.
“HSV1 could account for 50% or more of Alzheimer’s disease cases,” says Professor Ruth Itzhaki, an Alzheimer’s expert who has spent over 25 years at the University of Manchester in England investigating a potential link.
Itzhaki has shown previously that cold sores, caused by HSV1, occur more frequently in carriers of APOE-ε4 — a gene variant that confers increased risk of Alzheimer’s.
“Our theory is that in APOE-ε4 carriers, reactivation is more frequent or more harmful in HSV1-infected brain cells, which as a result accumulate damage that culminates in development of Alzheimer’s.”
Taiwan is one of the few countries in the world to collect the population data needed to test the HSV1-Alzheimer’s theory. There, 99.9 percent of the population is enrolled in a National Health Insurance Research Database, which is being extensively mined for information on microbial infections and disease.
In 2017-2018 three studies were published describing Taiwanese data on the development of senile dementia — of which Alzheimer’s is the main cause — and the treatment of patients with marked overt signs of infection with HSV or varicella zoster virus (VZV, the chickenpox virus).
“The striking results include evidence that the risk of senile dementia is much greater in those who are infected with HSV, and that anti-herpes antiviral treatment causes a dramatic decrease in number of those subjects severely affected by HSV1 who later develop dementia.”
Previous findings from Itzhaki’s research provide a mechanistic link which supports these epidemiological findings. Her research team found that HSV1 causes protein deposits characteristic of Alzheimer’s, including ‘plaques’ between neurons and ‘tangles’ inside of them.
“Viral DNA is located very specifically within plaques in postmortem brain tissue from Alzheimer’s sufferers. The main proteins of both plaques and tangles accumulate also in HSV1-infected cell cultures — and antiviral drugs can prevent this,” Itzhaki says.
“It should be stressed that the results of these Taiwanese studies apply only to severe HSV1 (or VZV) infections, which are rare,” Itzhaki says. “Ideally, we would study dementia rates amongst people who have suffered mild HSV1 infection, including herpes labialis (cold sores) or mild genital herpes, but these are far less likely to be documented.”
Although more research is needed to confirm and define a causal link between HSV1 infection and Alzheimer’s, Itzhaki is enthusiastic about the treatment prospects.
“Considering that over 150 publications strongly support an HSV1 role in Alzheimer’s, these Taiwan findings greatly justify usage of antiherpes antivirals — which are safe and well-tolerated — to treat Alzheimer’s disease.”