At this point there is no direct relationship established between propolis and stopping Alzheimer’s disease and other degenerative cognitive conditions, but there is emerging research that shows a link between herpes viruses and the development of dementia later in life.
In clinical study shows that patients treated with anti-herpes medications reduced their risk of developing dementia by 90 percent. One of the best natural anti-viral medicines available is propolis, specifically clinically studied Propolis GH2002.
Propolis is collected by bees from nearby trees and flowers for the construction and protection of the hive, (its Greek name means “defender of the city”) and has long been regarded as a powerful source of polyphenol compounds that boost the immune system and protect us from viral and bacterial invaders.
Nonetheless, the propolis extract called GH2002 is purified to remove wax and concentrate its beneficial compounds so it can provide consistent positive results, which it has done against both herpes simplex 1 and herpes simplex 2.
One of the reasons that herpes can affect cognitive strength later in life is that the herpes simplex 1 virus will “retreat” for a time into the brain of an individuals who are more prone to it reactivating later. Because propolis is a strong virus fighter it is possible that it could suppress and stop herpes viruses to the point where they are not only unlikely to break out again, but are no threat to the mind, either.
Itzhaki RF. Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s disease. Front Aging Neurosci, 19 October 2018
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.
Itzhaki RF, Lathe R. Herpes Viruses and Senile Dementia: First Population Evidence for a Causal Link. J Alzheimers Dis. 2018;64(2):363-366. doi: 10.3233/JAD-180266.
Three articles have very recently appeared that are of especial relevance to the causes of dementia and its potential treatment. The first two (Tsai et al., published in PLoS One in November 2017; Chen et al., published in the January/February 2018 issue of Journal of Clinical Psychiatry) demonstrate an increased risk of subsequent senile dementia (SD) development in patients with acute varicella zoster (herpes zoster) infection. These articles present data highly relevant to the third, and most important, paper-by Tzeng et al., published online in the journal Neurotherapeutics at the end of February 2018. These authors report that infection with a different herpes virus, herpes simplex virus type 1 (HSV1), leads to a similarly increased risk of later developing SD. Further, when the authors looked at patients treated aggressively with antiherpetic medications at the time, the relative risk of SD was reduced by a factor of 10. It should be stressed that no investigations were made on subjects already suffering from SD, and that those treated were the few rare cases severely affected by HSV. Nonetheless, antiherpetic medication prevented later SD development in 90% of their study group. These articles provide the first population evidence for a causal link between herpes virus infection and senile dementia.
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