Authors
Ji-Yeun Hur
Published in
Frontiers in aging neuroscience. Volume 18. Pages 1858017. Epub Aug 20, 2026.
Abstract
Over 95% of Alzheimer's disease (AD) is caused by a complex mixture of genetic and environmental factors. This is called sporadic AD or late-onset AD, and much of its pathological mechanisms remain unclear. There is growing evidence indicating that the viral infection, such as herpes simplex virus type 1 (HSV-1), triggers and worsens the AD progression in combination with the APOE4 genotype in AD patients. The innate immunity of host cells produces proinflammatory cytokines, which further drive neuroinflammation in the brain. Concurrently, Aβ and phosphorylated tau could entrap foreign pathogens such as HSV-1 according to the "antimicrobial protection hypothesis of AD," and accelerate the progression of AD. In this review, growing evidence ranging from HSV-1 infection to the AD progression via the accumulation of Aβ and tau, and neuroinflammation is explored.
PMID:
42694660
Bibliographic data and abstract were imported from PubMed on 04 Sep 2026.
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