Ruth F. Itzhaki- Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom
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..
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