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MINI REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1590909
This article is part of the Research TopicIntegrative AI and Multi-Omics: Precision Medicine in Immuno-InflammationView all 4 articles
The Role of Monocytes and Macrophages in the Progression of Alzheimer's Disease
Provisionally accepted- 1School of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130117, China, changchun, China
- 2Department of Pediatrics, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China, Urumqi, China
- 3State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Urumqi, 830054, China, Urumqi, China
- 4School of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 301617, China, Tianjin, China
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) plaques, neurofibrillary tangles (NFTs), and neuroinflammation. Monocytes and macrophages, particularly microglia, play a dual role in AD pathogenesis. In the early stages, they delay disease progression by phagocytosing Aβ, but chronic activation leads to Aβ accumulation and exacerbated neuroinflammation. Monocyte chemoattractant protein 1 (MCP-1) is a key regulator in neuroinflammation, Aβ deposition, and tau pathology, making it a potential therapeutic target. Moreover, recent breakthroughs in fluid and imaging biomarkers and targeted immunomodulatory agents underscore the growing importance of early diagnostic and therapeutic interventions. This review explores the complex interplay between monocytes, macrophages, and AD pathology, highlighting their roles in neuroinflammation, Aβ metabolism, and tau phosphorylation. Understanding these mechanisms offers new insights into developing effective diagnostic biomarkers and therapeutic strategies for AD.
Keywords: Alzheimer's disease, Monocytes, Macrophages, Neuroinflammation, β-Amyloid, MCP-1
Received: 10 Mar 2025; Accepted: 07 Apr 2025.
Copyright: © 2025 Nie, Yue and Hu. 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: Jingqing Hu, School of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130117, China, changchun, 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.