The viral hypothesis: how herpesviruses may contribute to Alzheimer's disease.
Journal
Molecular psychiatry
ISSN: 1476-5578
Titre abrégé: Mol Psychiatry
Pays: England
ID NLM: 9607835
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
received:
14
12
2020
accepted:
19
04
2021
revised:
12
04
2021
pubmed:
12
5
2021
medline:
3
2
2022
entrez:
11
5
2021
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 33972690
doi: 10.1038/s41380-021-01138-6
pii: 10.1038/s41380-021-01138-6
pmc: PMC8758477
doi:
Substances chimiques
Amyloid beta-Peptides
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
5476-5480Subventions
Organisme : NIA NIH HHS
ID : R01 AG062514
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG067193
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG063068
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG061835
Pays : United States
Informations de copyright
© 2021. The Author(s).
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