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REVIEW article
Front. Immunol.
Sec. Molecular Innate Immunity
Volume 15 - 2024 |
doi: 10.3389/fimmu.2024.1484373
This article is part of the Research Topic Application of Multi-omics Analyses in Revealing the Role of Mitochondrial Gene Defects in Disease Progression View all 13 articles
Mitochondrial Dysfunction in Alzheimer's Disease: A Key Frontier for Future Targeted Therapies
Provisionally accepted- 1 College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China
- 2 Department of Neurology, The Fourth People's Hospital of Jinan, Jinan, China
- 3 Department of Internal Medicine, Jinan Authority Hospital, Jinan, China
Alzheimer's disease (AD) is the most common neurodegenerative disorder, accounting for approximately 70% of dementia cases worldwide. Patients gradually exhibit cognitive decline, such as memory loss, aphasia, and changes in personality and behavior. Research has shown that mitochondrial dysfunction plays a critical role in the onset and progression of AD. Mitochondrial dysfunction primarily leads to increased oxidative stress, imbalances in mitochondrial dynamics, impaired mitophagy, and mitochondrial genome abnormalities. These mitochondrial abnormalities are closely associated with amyloid-beta and tau protein pathology, collectively accelerating the neurodegenerative process. This review summarizes the role of mitochondria in the development of AD, the latest research progress, and explores the potential of mitochondria-targeted therapeutic strategies for AD. Targeting mitochondria-related pathways may significantly improve the quality of life for AD patients in the future.
Keywords: Mitochondria, AD, dysfunction, mechanisms, therapeutic targets
Received: 21 Aug 2024; Accepted: 20 Dec 2024.
Copyright: © 2024 Wang, Liao, Zhang, Han, Liu and Wang. 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:
Zuning Liao, Department of Neurology, The Fourth People's Hospital of Jinan, Jinan, China
Qiying Zhang, Department of Internal Medicine, Jinan Authority Hospital, Jinan, China
Xinyuan Han, College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China
Changqing Liu, College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China
Jin Wang, College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China
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