Affiliations: [a]
Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Jilin University, Changchun, China
| [b]
Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China
Correspondence:
[*]
Correspondence to: Li Sun, Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Jilin University, Xinmin Street 71#, 130021, Changchun, China. Tel.: +86 13504313689; Fax: +86 432 88782161; E-mail: sunli99@jlu.edu.cn.
Abstract: Alzheimer’s disease (AD) is the most prevalent cause of dementia, accounting for approximately 60%–80%of all cases. Although much effort has been made over the years, the precise mechanism of AD has not been completely elucidated. Recently, great attention has shifted to the roles of iron metabolism, lipid peroxidation, and oxidative stress in AD pathogenesis. We also note that these pathological events are the vital regulators of a novel regulatory cell death, termed ferroptosis—an iron-dependent, oxidative, non-apoptotic cell death. Ferroptosis differs from apoptosis, necrosis, and autophagy with respect to morphology, biochemistry, and genetics. Mounting evidence suggests that ferroptosis may be involved in neurological disorders, including AD. Here, we review the underlying mechanisms of ferroptosis; discuss the potential interaction between AD and ferroptosis in terms of iron metabolism, lipid peroxidation, and the glutathione/glutathione peroxidase 4 axis; and describe some associated studies that have explored the implication of ferroptosis in AD.
