What is it about?
It is concerned with describing studies that support the concept that herpes simplex virus type 1 (HSV1) is present in dormant form in the brain of many elderly people, and that in brain of those who have a specific genetic factor, it confers a major risk of Alzheimer’s disease (AD). The number of supportive publications is increasing steadily, including support for the likelihood that reactivation of the dormant HSV1 occurs in the elderly brain (caused by events such as stress or by other infections), leading to an active HSV1 infection in the brain and consequent though limited damage. It is proposed that repeated reactivation causes cumulative damage and leads eventually to the development of AD.
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Why is it important?
There is evidence that suggests that treatment with antiherpes antiviral agents could protect the brain against damage by HSV1. No successful treatment for AD has yet been found, so if funding for a a clinical trial were to be obtained and if it were successful, this would be of very great importance both for patients and their carers, and also in reducing the enormous economic costs of the disease.
Perspectives
I am glad that this review and a much more recent one (in Frontiers of Aging Neuroscience) are in print because there has been a huge amount of opposition to the concept of a viral cause in Alzheimer's disease, although the opponents (many of whom are, unfortunately, very influential) never provide any scientific objections so they obviously have none. This hostility has made it extremely difficult for me and for others who have more recently started work in this line, to get funding and papers published on our research. I hope that the evidence provided in both reviews will help to make the viral concept accepted by doubters.
Ruth Itzhaki
University of Manchester
Read the Original
This page is a summary of: Herpes simplex virus type 1 and Alzheimer’s disease: possible mechanisms and signposts, The FASEB Journal, August 2017, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201700360.
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