Reviewing the Evidence for HSV1 to Contribute to Alzheimer's Disease

Alzheimer's disease starts with a slow rise in levels of amyloid-β present in the brain, an imbalance between dynamic processes of creation and clearance. This produces a state of mild biochemical and cognitive dysfunction that sets the stage for the later, much more destructive phase characterized by chronic inflammation, deposition of altered tau protein, and cell death. The roots of Alzheimer's must lie in the early mechanisms, in the poorly studied initial years of the condition, that cause some people to accumulate amyloid-β at a faster pace. In recent years evidence has emerged for persistent viral infection to play a role. Amyloid-β is coming to be seen as an anti-viral mechanism, and its creation and aggregation is prompted by the presence of viral particles.

Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer's disease (AD). This concept proposes that latent HSV1 in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE-ε4) is reactivated intermittently by events such as immunosuppression, peripheral infection, and inflammation, the consequent damage accumulating, and culminating eventually in the development of AD.

Population data to investigate this epidemiologically, e.g., to find if subjects treated with antivirals might be protected from developing dementia - are available in Taiwan, from the National Health Insurance Research Database, in which 99.9% of the population has been enrolled. This is being extensively mined for information on microbial infections and disease. Three publications have now appeared describing data on the development of senile dementia (SD), and the treatment of those with marked overt signs of disease caused by varicella zoster virus (VZV), or by HSV. The striking results show that the risk of SD is much greater in those who are HSV-seropositive than in seronegative subjects, and that antiviral treatment causes a dramatic decrease in number of subjects who later develop SD.

It should be stressed that these results apply only to those with severe cases of HSV1 or VZV infection, but when considered with the over 150 publications that strongly support an HSV1 role in AD, they greatly justify usage of antiherpes antivirals to treat AD.

Link: https://doi.org/10.3389/fnagi.2018.00324

Comments

Just a thought for those worried about HSV: You can get a battery of shots over the counter in Russia that will knock out just about everything. This is like a neutron bomb, so you have to follow up with probiotics to get back to normal. I remember the pain and strange intimacy of the wife and I giving each other injections in the rump.

Posted by: Tom Schaefer at October 22nd, 2018 7:30 AM

@Tom
Antibiotics so nothing against viruses. They might help with some opportunistic companion infections, though...

Antiviral medications are not that powerful. Tamiflu bruns marginal benefits for people withe weaker immunity like the elderly...

Posted by: Cuberat at October 22nd, 2018 5:46 PM

Just to speculate --

Data from Finland and Japan seem to show that both saunas and hot baths significantly reduce Alzheimer's incidence. Since exposure to heat appears to assist the immune system in clearing viruses, could it also be a therapy against HSV and Alzheimer's?

Posted by: L Pagnucco at October 26th, 2018 11:39 AM

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