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REVIEW article
Front. Aging Neurosci.
Sec. Alzheimer's Disease and Related Dementias
Volume 17 - 2025 | doi: 10.3389/fnagi.2025.1499871
This article is part of the Research Topic Current Chemical Approaches in Combating Neuroinflammation in Alzheimer's Disease (AD) View all 5 articles
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline and neuronal degeneration. Emerging evidence implicates necroptosis in AD pathogenesis, driven by the RIPK1-RIPK3-MLKL pathway, which promotes neuronal damage, inflammation, and disease progression. Exercise, as a non-pharmacological intervention, can modulate key inflammatory mediators such as TNF-α, HMGB1, and IL-1β, thereby inhibiting necroptotic signaling. Additionally, exercise enhances O-GlcNAc glycosylation, preventing Tau hyperphosphorylation and stabilizing neuronal integrity. This review explores how exercise mitigates necroptosis and neuroinflammation, offering novel therapeutic perspectives for AD prevention and management.
Keywords: Alzheimer's disease, necroptosis, Exercise, Neuronal degeneration, Cognitive Function
Received: 22 Sep 2024; Accepted: 15 Jan 2025.
Copyright: © 2025 Lu, Zhao and Tan. 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:
Donglei Lu, Tianjin University of Sport, Tianjin, China
Sijie Tan, Tianjin University of Sport, Tianjin, 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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