The University of Manchester scientists have shown that the herpes simplex virus type 1 (HSV1) is a risk factor for the neurodegenerative disorder Alzheimer's when it is present in the brains of people who have a specific genetic risk to the disease. In other words, HSV1, together with the host genetic factor, is a major risk for the disease. The herpes virus has been shown to cause the accumulation of two significant AD proteins: β-amyloid (Aβ) and abnormally phosphorylated tau (P-tau), known to be the main components of plaques and tangles. Both proteins are thought by many scientists to be involved in the development of AD.
According to Prof. Itzhaki, the team leader in the University's Faculty of Life Sciences, "the viral DNA in AD brains is very specifically located within amyloid plaques. This, together with the production of amyloid that the virus induces, suggests that HSV1 is a cause of toxic amyloid products and of plaques." These results therefore suggest that a possible effective treatment of AD (to slow disease progression at least) would be to use antiviral agents to target the replication of HSV1 DNA. This would be successful only if the accumulation of β-amyloid and P-tau caused by the virus occurs at or after the stage at which viral DNA replication occurs.
- Julie Saffarian
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