Glycogen Synthase Kinase-3β, NLRP3 Inflammasome, and Alzheimer's Disease.
Alzheimer’s disease
NLRP3 inflammasome
glycogen synthase kinase-3β
Journal
Current medical science
ISSN: 2523-899X
Titre abrégé: Curr Med Sci
Pays: China
ID NLM: 101729993
Informations de publication
Date de publication:
Oct 2023
Oct 2023
Historique:
received:
11
06
2023
accepted:
25
07
2023
pubmed:
18
9
2023
medline:
18
9
2023
entrez:
18
9
2023
Statut:
ppublish
Résumé
Alzheimer's disease (AD) is the most prevalent cause of dementia worldwide. Because of the progressive neurodegeneration, individual cognitive and behavioral functions are impaired, affecting the quality of life of millions of people. Although the exact pathogenesis of AD has not been fully elucidated, amyloid plaques, neurofibrillary tangles (NFTs), and sustaining neuroinflammation dominate its characteristics. As one of the major tau kinases leading to hyperphosphorylation and aggregation of tau, glycogen synthase kinase-3β (GSK-3β) has been drawing great attention in various AD studies. Another research focus of AD in recent years is the inflammasome, a multiprotein complex acting as a regulator in immunological reactions to exogenous and endogenous danger signals, of which the Nod-like receptor (NLR) family, pyrin domain-containing 3 (NLRP3) inflammasome has been studied mostly in AD and proven to play a significant role in AD development by its activation and downstream effects such as caspase-1 maturation and interleukin (IL)-1β release. Studies have shown that the NLRP3 inflammasome is activated in a GSK-3β-dependent way and that inhibition of the NLRP3 inflammasome downregulates GSK-3β, suggesting that these two important proteins are closely related. This article reviews the respective roles of GSK-3β and the NLRP3 inflammasome in AD as well as their relationship and interaction.
Identifiants
pubmed: 37721665
doi: 10.1007/s11596-023-2788-4
pii: 10.1007/s11596-023-2788-4
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
847-854Informations de copyright
© 2023. Huazhong University of Science and Technology.
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