Mounting Evidence Suggests That The Herpes Virus Causes Alzheimer’s

U.S. Department of Energy/Public Domain


More than 30 million people worldwide suffer from Alzheimer's disease, and new treatments could be on the horizon.

Evidence is mounting that the herpes virus could be a cause of Alzheimer’s disease — the most common type of dementia — which suggest that the condition could be treated with antiviral medications, and it might even be possible to vaccinate children against it.

Ruth Itzhaki, Professor Emeritus of Molecular Neurobiology at the University of Manchester, said the virus linked to Alzheimer’s is herpes simplex virus type 1 (HSV1), most commonly known as the virus behind cold sores.

It infects most people in infancy and then remains dormant in the peripheral nervous system (the part of the nervous system that isn’t the brain and the spinal cord). Occasionally, if a person is stressed, the virus becomes activated and, in some people, it causes cold sores.

We discovered in 1991 that in many elderly people HSV1 is also present in the brain. And in 1997 we showed that it confers a strong risk of Alzheimer’s disease when present in the brain of people who have a specific gene known as APOE4.

Itzhaki said the virus can become active in the brain, and she contends after what is likely repeated activations, the brain sustains cumulative damage. Carriers of APOE4 who also have HSVI in the brain are 12 times more likely to develop Alzheimer’s disease than those with neither factor.

Later, we and others found that HSV1 infection of cell cultures causes beta-amyloid and abnormal tau proteins to accumulate. An accumulation of these proteins in the brain is characteristic of Alzheimer’s disease.

We believe that HSV1 is a major contributory factor for Alzheimer’s disease and that it enters the brains of elderly people as their immune system declines with age. It then establishes a latent (dormant) infection, from which it is reactivated by events such as stress, a reduced immune system and brain inflammation induced by infection by other microbes.

Reactivation leads to direct viral damage in infected cells and to viral-induced inflammation. We suggest that repeated activation causes cumulative damage, leading eventually to Alzheimer’s disease in people with the APOE4 gene.

Itzhaki stressed that the studies to date point only to a correlation between the herpes virus and Alzheimer’s disease and not causation — but it does open the door to new treatments.

The data suggest that antiviral agents might be used for treating Alzheimer’s disease. The main antiviral agents, which are safe, prevent new viruses from forming, thereby limiting viral damage.

In an earlier study, we found that the anti-herpes antiviral drug, acyclovir, blocks HSV1 DNA replication, and reduces levels of beta-amyloid and tau caused by HSV1 infection of cell cultures.

Excitingly, successful prevention of Alzheimer’s disease by use of specific anti-herpes agents has now been demonstrated in a large-scale population study in Taiwan. Hopefully, information in other countries, if available, will yield similar results.


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