Mini-Review: Is iron-mediated cell death (ferroptosis) an identical factor contributing to the pathogenesis of some neurodegenerative diseases?

• Published in: Neuroscience letters 2021-02, Vol.745, p.135627-135627, Article 135627
• Main Authors: Viktorinova, Alena, Durfinova, Monika
• Format: Article
• Language: English
• Subjects: Animals; Cell Death - drug effects; Cell Death - physiology; Demyelination; Ferroptosis; Ferroptosis - drug effects; Ferroptosis - physiology; Humans; Iron - metabolism; Iron Chelating Agents - pharmacology; Iron Chelating Agents - therapeutic use; Iron dyshomeostasis; Iron Overload - epidemiology; Iron Overload - metabolism; Iron Overload - therapy; Lipid peroxidation; Neurodegeneration; Neurodegenerative Diseases - epidemiology; Neurodegenerative Diseases - metabolism; Neurodegenerative Diseases - therapy; Reactive Oxygen Species - antagonists & inhibitors; Reactive Oxygen Species - metabolism
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2021.135627

[Display omitted] •Iron dyshomeostasis (especially iron overload) is a critical condition of neurodegeneration.•Some neurodegenerative diseases can be accompanied by ferroptosis.•Iron dysregulation, lipid-generated ROS, and ferroptosis are identical features of diverse neurodegenerative diseases. The review article briefly discusses a hypothesis based on the potential participation of iron dyshomeostasis and iron-mediated cell death (ferroptosis) in the pathogenesis of some neurodegenerative diseases. Iron dyshomeostasis (especially cellular iron overload) is considered to be a critical condition of neurodegeneration. The etiopathogenesis of many neurodegenerative diseases including Alzheimer's and Parkinson's diseases, Multiple sclerosis, and others, is different. However, there are several identical cellular processes, such as iron dyshomeostasis (an excessive iron deposition), iron-induced oxidative stress, the accumulation of lipid-generated reactive oxygen species, and ferroptosis that accompany these diseases. Based on the existing theoretical and experimental evidence, the article provides current insight into iron dyshomeostasis and ferroptosis as a contributing factor to the pathogenesis of neurodegeneration. In addition, special attention is addressed to the possible relationship between cellular iron overload and key pathological features of selected neurodegenerative diseases, such as β-amyloid and tau proteins, α-synuclein, and demyelination. The mechanism by which ferroptosis may be involved in the pathogenesis of various neurodegenerative diseases is not fully elucidated. Further experimental and clinical studies are needed to clarify the hypothesis on the potential role of ferroptosis in the pathogenesis of neurodegenerative diseases.