Journal of NeuroVirology

, Volume 14, Issue 1, pp 1–4

Herpes simplex virus type 1 and Alzheimer’s disease: The autophagy connection

Authors

    • Faculty of Life Sciences (North Campus)The University of Manchester, Moffat Building
  • S. Louise Cosby
    • Division of Infection and Immunity (CCRCB)Queen’s University Belfast
  • Matthew A. Wozniak
    • Faculty of Life Sciences (North Campus)The University of Manchester, Moffat Building
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DOI: 10.1080/13550280701802543

Cite this article as:
Itzhaki, R.F., Cosby, S.L. & Wozniak, M.A. Journal of NeuroVirology (2008) 14: 1. doi:10.1080/13550280701802543
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Abstract

The causes of Alzheimer’s disease (AD) and of the characteristic pathological features—amyloid plaques and neurofibrillary tangles—of AD brain are unknown, despite the enormous resources provided over the years for their investigation. Indeed, the only generally accepted risk factors are age, Down syndrome, carriage of the type 4 allele of the apolipoprotein E gene (APOE-ε4), and possibly brain injury. Following the authors’ previous studies implicating herpes simplex virus type 1 (HSV1) in brain of APOE-ε4 carriers as a major cause of AD, the authors propose here, on the basis of their and others’ recent studies, that not only does HSV1 generate the main components of amyloid plaques and neurofibrillary tangles (NFTs)—β-amyloid (Aβ) and abnormally phosphorylated tau but also, by disrupting autophagy, it prevents degradation of these aberrant proteins, leading to their accumulation and deposition, and eventually to AD.

Keywords

Alzheimer’s diseaseamyloidautophagyherpes simplex virus type 1ICP34.5tau

Copyright information

© Journal of NeuroVirology, Inc. 2008