New research shows evidence of the fundamental link between herpes viruses and Alzheimer’s, igniting possibilities for further research and treatment.
The review available in Frontiers in Ageing Neuroscience raises the prospect of a simple, effective preventive treatment for one of humanity’s most harmful disorders. Cold sores caused by herpes viruses could indeed lead to Alzheimer’s disease – and new data shows antiviral drugs drastically reduce risk of senile dementia in patients with severe herpes infections.
The theory behind the link
Herpes viruses remain lifelong in our neurons and immune cells, reactivating and resurfacing in distinctive blisters when an individual is run down by stress or illness. Many individuals are infected by Herpes Simplex Virus 1 (HSV1) by the time they reach old age.
Professor Itzhaki, from the University of Manchester, UK, said: “HSV1 could account for 50% or more of Alzheimer’s disease cases.”
HSV1 is better known as the cause of cold sores, research has shown previously that cold sores occur more frequently in carriers of APOE-ε4, which is a gene variant that confers increased risk of Alzheimer’s.
Itzhaki further explains: “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.”
Proving the theory
Not many countries gather information regarding the population data required to test this theory.
However, researchers in Taiwan discovered that 99.9% 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.
“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 own research group provide a mechanistic link which supports these epidemiological findings. They found that herpes viruses cause protein deposits similar to that of Alzheimer’s, describing them to be ‘plaques’ between neurons and ‘tangles’ inside of them.
Itzhaki goes on to explain that “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.”
Prospects of a cure
Although additional work is needed to confirm and define the fundamental link between herpes viruses and Alzheimer’s, Itzhaki emphasises: “It should be stressed that the results of these Taiwanese studies apply only to severe HSV1 (or VZV) infections, which are rare.”
“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.”
The researchers, however are 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.