Herpes could be a cause of Alzheimer's disease – here's why



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More than 30 million people around the world suffer from Alzheimer's disease – the most common form of dementia. Unfortunately, there is no cure, there are only medications to relieve the symptoms. However, my last exam suggests a way to treat the disease. I have found the strongest evidence to date that the herpes virus is a cause of Alzheimer's disease, suggesting that safe and effective antiviral drugs may be able to treat the disease. We might even be able to vaccinate our children against it.

The virus involved in Alzheimer's disease, the herpes simplex virus type 1 (HSV1), is best known for causing cold sores. It infects most young people and then remains dormant in the peripheral nervous system (the part of the nervous system that is neither the brain nor the spinal cord). Sometimes, if a person is stressed, the virus is active and, in some people, it causes cold sores.

We discovered in 1991 that HSV1 is also present in the brain in many elderly people. And in 1997, we showed that it confers a high risk of Alzheimer's disease when it is present in the brain of people with a specific gene called APOE4.

The virus can become active in the brain, perhaps several times, which probably causes cumulative damage. The probability of developing Alzheimer's disease is 12 times greater in APOE4 carriers with HSV1 in the brain than in those without any factor.

Later, we and others discovered that an HSV1 infection of cell cultures results in an accumulation of beta-amyloid and abnormal tau proteins. The accumulation of these proteins in the brain is characteristic of Alzheimer's disease.

We believe that HSV1 is a major contributor to Alzheimer's disease and that it enters the brains of older people as their immune systems deteriorate with age. It then establishes a latent (dormant) infection from which it is reactivated by events such as stress, a decrease in the immune system and inflammation of the brain 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.

Presumably, in APOE4 carriers, Alzheimer’s disease develops in the brain because of greater HSV1-induced formation of toxic products, or less repair of damage.

New treatments?

The data suggests 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.


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It’s important to note that all studies, including our own, only show an association between the herpes virus and Alzheimer’s – they don’t prove that the virus is an actual cause. Probably the only way to prove that a microbe is a cause of a disease is to show that an occurrence of the disease is greatly reduced either by targeting the microbe with a specific anti-microbial agent or by specific vaccination against the microbe.

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.

Ruth Itzhaki is a professor emeritus of molecular neurobiology at the University of Manchester. This article first appeared on The Conversation (theconversation.com)

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