A new commentary by scientists at the universities of Manchester and Edinburgh, UK, on a study by Taiwanese epidemiologists has shown support for the link between the herpes virus and reduced risk of Alzheimer’s disease.
After looking at subjects who suffered from the herpes virus and were treated aggressively with antiviral drugs, Taiwanese authors discovered that the relative risk of dementia was reduced by a factor of 10.
Manchester’s Professor Ruth Itzhaki and Edinburgh’s Professor Richard Lathe say the paper, by Tzeng et al. and published in Neurotherapeutics in February 2018, also shows that herpes simplex virus type 1 (HSV1) leads to an increased risk of developing the neurodegenerative disease.
Itzhaki commented: “This article and two others by different research groups in Taiwan provide the first population evidence for a causal link between herpes virus infection and Alzheimer’s disease, a hugely important finding.”
The strongest evidence yet for herpes virus and dementia link
A commentary in the Journal of Alzheimer’s Disease on the three articles was published, which argued that they provide the strongest evidence for a casual link between herpes infection and Alzheimer’s disease, which backed 30 years of Itzhaki’s research.
Itzhaki added: “I believe we are the first to realise the implications of these striking data on this devastating condition which principally affects the elderly. No effective treatments are yet available.
“Almost 30 million people worldwide suffer from it and sadly, this figure will rise as longevity increases.
“But we believe that these safe and easily available antivirals may have a strong part to play in combating the disease in these patients.
“It also raises the future possibility of preventing the disease by vaccination against the virus in infancy.
“Successful treatment by a specific drug, or successful vaccination against the putative microbe, are the only ways to prove that a microbe is the cause of a non- infectious human disease.”
How does HSV1 infect humans?
HSV1 infects most humans in youth or later and remains dormant within the peripheral nervous system. From time to time the virus becomes activated and, in some individuals, it can cause visible damage in the form of cold sores.
In the study, it was found that the risk of developing dementia in the group with severe HSV was increased by a factor of 2.542 but, when the authors compared those among the HSV cohort who were treated with antiviral therapy versus those who did not receive it, there was a substantial tenfold reduction in the later incidence of dementia over 10 years.
Lathe added: “Not only is the magnitude of the antiviral effect remarkable, but also the fact that—despite the relatively brief duration and the timing of treatment—in most patients severely affected by HSV1 it appeared to prevent the long-term damage in brain that results in Alzheimer’s.”
Is the evidence of Alzheimer’s and HSV1 definitive?
Itzhaki concluded: “It was as long ago as 1991 when we discovered that, in many elderly people infected with HSV1, the virus is present also in the brain, and then in 1997 that it confers a strong risk of Alzheimer’s disease in the brain of people who have a specific genetic factor.
“In 2009, we went on to show that HSV DNA is inside amyloid plaques in Alzheimer’s patients’ brains.
“We suggested that the virus in brain is reactivated by certain events such as stress, immunosuppression, and infection/inflammation elsewhere.
“So, we believe the cycle of HSV1 reactivation in the brain eventually causes Alzheimer’s in at least some patients.”
In addition to Itzhaki’s work suggesting a connection between HSV-1 and plaques in Alzheimer’s brain tissue, there is also a recent report by Redhead et al of a connection between overexpression of HHV-6A and HHV-7 DNA in genomic extracts from Alzheimer’s brains. “The game is still afoot”, as Sherlock might have said.