Neural Regeneration Research ›› 2024, Vol. 19 ›› Issue (8): 1741-1750.doi: 10.4103/1673-5374.389362

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Ferroptosis mechanism and Alzheimer’s disease

Lina Feng1, Jingyi Sun1, Ling Xia1, Qiang Shi1, Yajun Hou1, Lili Zhang2, Mingquan Li3, *, Cundong Fan1, *, Baoliang Sun1, *   

  1. 1Shandong Key Laboratory of TCM Multi-Target Intervention and Disease Control, the Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong Province, China; 2Department of Internal Medicine, Taian Traffic Hospital, Taian, Shandong Province, China; 3Department of Neurology, the Third Affiliated Clinical Hospital of Changchun University of Chinese Medicine, Changchun, Jilin Province, China
  • Online:2024-08-15 Published:2024-01-03
  • Contact: Mingquan Li, PhD, Limingquan0001@126.com; Cundong Fan, PhD, cdfan@sdfmu.edu.cn; Baoliang Sun, PhD, tblsun66@163.com.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, No. 81501106 (to CF), Fund of Taishan Scholar Project (to CF); the Natural Science Foundation of Shandong Province, No. ZR2020QH106 (to YH) and the Medical and Health Science and Technology Development Plan of Shandong Province, No. 202203010799 (to QS).

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Abstract: Regulated cell death is a genetically determined form of programmed cell death that commonly occurs during the development of living organisms. This process plays a crucial role in modulating homeostasis and is evolutionarily conserved across a diverse range of living organisms. Ferroptosis is a classic regulatory mode of cell death. Extensive studies of regulatory cell death in Alzheimer’s disease have yielded increasing evidence that ferroptosis is closely related to the occurrence, development, and prognosis of Alzheimer’s disease. This review summarizes the molecular mechanisms of ferroptosis and recent research advances in the role of ferroptosis in Alzheimer’s disease. Our findings are expected to serve as a theoretical and experimental foundation for clinical research and targeted therapy for Alzheimer’s disease.

Key words: Alzheimer’s disease, apolipoprotein E, Fe2+, ferroptosis, glial cell, glutathione peroxidase 4, imbalance in iron homeostasis, lipid peroxidation, regulated cell death, system Xc–