The herpes virus could be linked to at least half of all Alzheimer’s disease cases, a scientist has claimed.
Professor Ruth Itzhaki, who has spent more than 25 years at the University of Manchester investigating a potential link between the two, said studies carried out in Taiwan suggested that the risk of dementia was much greater in those infected with herpes simplex virus (HSV).
There are two types of HSV: HSV1, also known as oral herpes, which causes cold sores and blisters around the mouth and on the face; and HSV2, which is generally responsible for genital herpes outbreaks.
“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,” Professor Itzhaki said.
“HSV1 could account for 50 per cent or more of Alzheimer’s disease cases.”
Prof Itzhaki used Taiwan for the research as 99.9 per cent of the population is enrolled in a National Health Insurance Research Database, which is being mined for information on microbial infections and disease.
In 2017/18, 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).
“It should be stressed that the results of these Taiwanese studies apply only to severe HSV1 (or VZV) infections, which are rare,” Professor Itzhaki said.
“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.”
Prof Itzhaki has previously shown that cold sores occur more frequently in carriers of APOE-?4 – a gene variant that increases the risk of Alzheimer’s.
“Our theory is that in APOE4 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,” Prof Itzhaki added.
“Viral DNA is located very specifically within plaques in post-mortem 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.”
The Alzheimer’s Society said the paper highlighted existing studies that suggest people who have the herpes virus infection may be more likely to develop dementia, but due to the nature of the research it does not show a cause and effect relationship between herpes and dementia.
The charity’s head of research Dr James Pickett said herpes is a “hot topic in dementia research”.
“As the infection appears to be more common in the brains of people with Alzheimer’s compared to healthy brains – but we don’t yet know enough about the relationship between the two,” Dr Pickett said.
“The link between herpes and dementia isn’t something that we feel people should worry about, although it’s sensible general advice to seek treatment for persistent cold sores.
He added dementia isn’t contagious and shouldn’t be thought of as an infectious disease.
“More research is needed to find out whether antiviral drugs can reduce dementia risk,” Dr Pickett said.
“Someone in the UK develops dementia every three minutes, and our scientists at the UK Dementia Research Institute are working hard to understand why, so that we can find ways to beat it.”
The research is published in Frontiers in Ageing Neuroscience.