The viral hypothesis: how herpesviruses may contribute to Alzheimer’s disease
Open accessAbstract
The hypothesis that infectious agents, particularly herpesviruses, contribute to Alzheimer’s disease (AD) pathogenesis has been investigated for decades but has long engendered controversy. In the past 3 years, several studies in mouse models, human tissue models, and population cohorts have reignited interest in this hypothesis. Collectively, these studies suggest that many of the hallmarks of AD, like amyloid beta production and neuroinflammation, can arise as a protective response to acute infection that becomes maladaptive in the case of chronic infection. We place this work in its historical context and explore its etiological implications.
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Infectious triggers and neurovascular dysfunction have been proposed as additional contributors to AD.
“More recently, infectious triggers [18, 19] and neurovascular dysfunction [20] have been proposed as additional contributors, broadening the scope of investigation and linking AD to systemic physiology.”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [19]
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APOE4, activation of latent form HSV-1, A beta accumulation and AD progression
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- Authors
- Wainberg, M., Luquez, T., Koelle, D. M., Readhead, B., Johnston, C., Darvas, M., & Funk, C. C.
- Affiliations
- Institute for Systems Biology (US)
- University of Washington (US)
- Arizona State University (US)
- Corresponding author
- Funk, Cory C.
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2021-05-10
- Volume
- 26
- Issue
- 10
- Pages
- 5476-5480
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC8758477
- OpenAlex
- W3160107726
- Cited by
- 74
- References
- 36
- Citations by year
- 2026: 20 · 2025: 25 · 2024: 11 · 2023: 9 · 2022: 4 · 2021: 5
- FWCI
- 0.97
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Molecular Psychiatry (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (U01AG061835, R01AG062514, R21AG063068)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, herpesvirus, viral hypothesis, infectious etiology, amyloid-beta, neuroinflammation, chronic infection, acute infection, mouse model, population cohort
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Herpesviridae, Amyloid beta-Peptides, Mice
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