The surprising relationship of herpes simplex with Alzheimer's disease (and what it entails to treat this mental illness) – BBC News



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More than 30 million people worldwide suffer from Alzheimer's disease, the most common form of dementia.

Unfortunately, there is no cure, only medications to relieve symptoms.

However, my own research I found the strongest evidence up to now that the herpes virus is a cause of the disease. # 39; Alzheimer's.

This suggests that the herpes virus is a cause of Alzheimer's disease. antivirals, effective and safe, could allow to treat the disease . We could even vaccinate our children against that.

The virus involved in Alzheimer's disease, Herpes simplex type 1 ( HSV1 ), is best known for causing pimples fever.

It infects most people during childhood and then remains dormant in the peripheral nervous system (the part of the nervous system other than the brain and spinal cord).

Sometimes, if a person is stressed, the virus is activated and, in some people, causes cold sores.

  Scanning images of the brain
Stress moments can reactivate the virus. Herpes can cause long-term brain damage.

We discovered in 1991 that HSV1 is also present in the brains of many older people.

And in 1997, we showed that it presented a great risk of development. Alzheimer's disease when it is present in the brain brother of people with a specific gene known as APOE4.

The virus can be activated in the brain, perhaps by repetition, which probably causes cumulative damage.

The likelihood of developing the disease Alzheimer's disease is 12-fold higher in APOE4 carriers with HSV1 in the brain than in those with no factor.

Later, we and others discovered this infection by HSV1 cell cultures. causes accumulation of abnormal beta-amyloid and tau proteins.

The accumulation of these proteins in the brain is characteristic of Alzheimer's disease .

The APOE4 Gene

We believe that the HSV1 gene is an important factor that contributes to Alzheimer's disease and enters the brains of the elderly as their immune systems weaken with the disease. # 39; age.

Then establishes a latent infection. (inactive), from which it is reactivated by events such as stress, a reduction of the immune system and inflammation of the brain induced by the infection of other microbes.

Reactivation results in direct viral damage to infected cells and inflammation.

  Illustration of damaged neuronal junctions
Alzheimer's disease is the most common form of dementia in the world, affecting some 30 million people.

We propose that repeated activation causes cumulative damage. which ultimately leads to Alzheimer's disease in people with the APOE4 gene.

It is hypothesized that in APOE4 carriers, Alzheimer's disease develops in the brain due to increased formation of toxic products induced by HSV1, or less repair of damage.

New treatments?

The data suggest that antiviral agents could be used to treat Alzheimer's disease.

The main antiviral agents, which are safe, prevent the formation of new viruses which limits the viral damage.

In a previous study, we had discovered that an anti-herpes antiviral drug, acyclovir, blocked replication of HSV1 DNA and reduced beta-amyloid and tau levels caused by infection of HSV1 cell cultures.

It is important to note that all studies, including ours, only show an badociation between the herpes virus and Alzheimer's disease.

They do not show that the virus is a real cause .

The only way to prove that a microbe is the cause of a disease is probably to demonstrate that the onset of the disease is significantly reduced by attacking the microbe with a specific antimicrobial agent or with a specific vaccination against the microbe.

An exciting and successful prevention of the disease. Alzheimer's disease using the use of specific agents against herpes has been demonstrated in a large-scale population study in Taiwan.

Hopefully the information available in other countries will yield results

* Ruth Itzhaki is Professor Emeritus of Molecular Neurobiology at the University of Manchester, England. This article was originally published in The Conversation and has been reissued under a Creative Commons license.


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