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MINI REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1583886
This article is part of the Research Topic Integrative AI and Multi-Omics: Precision Medicine in Immuno-Inflammation View all articles
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuroinflammation, with no definitive cure currently available. The NLRP3 inflammasome, a key mediator of neuroinflammation, has emerged as a critical player in AD pathogenesis, contributing to the accumulation of β-amyloid (Aβ) plaques, tau hyperphosphorylation, and neuronal damage. This review explores the mechanisms by which the NLRP3 inflammasome is activated in AD, including its interactions with Aβ, tau, reactive oxygen species (ROS), and pyroptosis. Additionally, it highlights the role of the ubiquitin system, ion channels, autophagy, and gut microbiota in regulating NLRP3 activation. Therapeutic strategies targeting the NLRP3 inflammasome, such as IL-1β inhibitors, natural compounds, and novel small molecules, are discussed as promising approaches to mitigate neuroinflammation and slow AD progression. This review underscores the potential of NLRP3 inflammasome inhibition as a therapeutic avenue for AD.
Keywords: NLRP3, Neuro-inflammation, IL-1β, Inflammasome, Alzheimer's disease, Microglia, Inhibitior
Received: 26 Feb 2025; Accepted: 19 Mar 2025.
Copyright: © 2025 Li and Gong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Chunrong Gong, Department of rehabilitation medicine, Linyi people's Hospital, Linyi, China, Linyi, Shandong Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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