Alzheimer’s may be infectious and not inherited.

Dr. Weeks’ Comment: Years ago, we taught our patients and readers that Alzheimer’s disease is a disease of inflammation prevented and optimally treated by safe and effective anti-inflammatory agents and also that the herpes virus is encapsulated in the lesions. Finally we maintained the obvious that all of the Alzheimer’s drugs are not helpful. Now, more research agrees and points us AWAY from the standard of care for the horrible dehumanizing disease. So what do we need? Safe and effective anti-inflammatory diet and low dose lithium with certain B vitamins optimizing certain minerals and transdermal bioidentical progesterone. (See this post re B vitamins for Alzheimer’s)

Front. Aging Neurosci., 19 October 2018 |

Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease

Ruth F. Itzhaki

INTRODUCTION: 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. Three other studies are described which directly relate to HSV1 and AD: they deal respectively with lysosomal changes in HSV1-infected cell cultures, with evidence for a role of human herpes virus type 6 and 7 (HHV6 and HHV7) in AD, and viral effects on host gene expression, and with the antiviral characteristics of beta amyloid (Aβ). Three indirectly relevant studies deal respectively with schizophrenia, relating to antiviral treatment to target HSV1, with the likelihood that HSV1 is a cause of fibromyalgia (FM), and with FM being associated with later development of SD. Studies on the link between epilepsy, AD and herpes simplex encephalitis (HSE) are described also, as are the possible roles of APOE-ε4, HHV6 and HSV1 in epilepsy.”

Even in the conclusion of this article she agrees that the science has been ignored: “… Research data on a microbial cause of AD have been ignored or dismissed for three decades..” Why? Well we can agree that the remedy for a viral infection is not very expensive. Remember the first rule of Corporate Medicine (i.e. medicine practiced for profit and not patients’ sake) – “If the solution is not remunerative, the problem doesn’t exist.”


Further population epidemiological work would be invaluable for understanding the role of microbes, in particular HSV1, in AD. Using the Taiwan records, or those of any other country with comparable information, the subsequent development of dementia amongst subjects who had suffered mild herpes labialis or genital herpes could be investigated, although they would be far less likely to be documented, and therefore much less identifiable than severe cases. However, investigation of even asymptomatic HSV-seropositive people vs. HSV-seronegative people would be informative, although by the age of 60 the latter would comprise only a very small minority. Also, individuals could be selected who had suffered severe peripheral infections, on the basis that the inflammation thus caused could lead to inflammation in the brain, and reactivation of any latent microbe there. Of particular interest would be those who had suffered HSE, and also epilepsy patients—even those in whom no virus infection had been reported. If tissue, blood, or salve samples were available, APOE genotypes could be determined for any association with other characteristics.

Clearly, the types of antiviral which might be used for treating AD should be carefully chosen, especially if combined with an anti-inflammatory agent, as well as the duration of treatment and stage at which their usage would most effective. Even if the effects were merely a delay in onset of the disease, this would still be enormously beneficial for patients, carers and the economy. Of course, vaccination against HSV1 would be the better option, as prevention of disease is better than cure. Unfortunately, however, there is currently no vaccine for HSV1 and any vaccine trial would presumably have to extend for many years to find the outcome.

Research data on a microbial cause of AD have been ignored or dismissed for three decades, very unfortunately for those who developed AD during that period and who therefore had no chance of benefitting from the information. Surely, now is the time to rectify the situation by determining and then using the best means of treatment at hand.

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