Affiliations: Department of Neuroscience and Center for Neurovirology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, USA
Correspondence:
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Correspondence to: Dr. Kamel Khalili, Department of Neuroscience and Center for Neurovirology, Lewis Katz School of Medicine at Temple University, 3500 North Broad Street, 7th Floor, Philadelphia, PA 19140, USA. Tel.: +1 215 707 4500; Fax: +1 215 707 4888; E-mail: kamel.khalili@temple.edu.
Abstract: Across the fields of virology and neuroscience, the role of neurotropic viruses in Alzheimer’s disease (AD) has received renewed enthusiasm, with a particular focus on human herpesviruses (HHVs). Recent genomic analyses of brain tissue collections and investigations of the antimicrobial responses of amyloid-β do not exclude a role of HHVs in contributing to or accelerating AD pathogenesis. Due to continued expansion in our aging cohort and the lack of effective treatments for AD, this composition examines a potential neuroviral theory of AD in light of these recent data. Consideration reveals a possible viral “Hit-and-Run” scenario of AD, as well as neurobiological mechanisms (i.e., neuroinflammation, protein quality control, oxidative stress) that may increase risk for AD following neurotropic infection. Although limitations exist, this theoretical framework reveals several novel therapeutic targets that may prove efficacious in AD.
