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.

这篇综述文章简要讨论了一种假说，该假说基于铁动态异常和铁介导的细胞死亡（肥大症）在某些神经退行性疾病的发病机理中的潜在参与。铁动态异常（特别是细胞铁超负荷）被认为是神经退行性变的关键条件。许多神经退行性疾病（包括阿尔茨海默氏病和帕金森氏病，多发性硬化症等）的病因病因不同。但是，存在几种相同的细胞过程，例如铁动态异常（铁沉积过多），铁诱导的氧化应激，脂质生成的活性氧种类的积累以及伴随这些疾病的肥大病。根据现有的理论和实验证据，这篇文章提供了关于铁动态异常和铁质异常的最新见解，铁质异常和铁质异常是神经退行性疾病发病机理的重要因素。此外，应特别注意细胞铁超负荷与某些神经退行性疾病的关键病理特征之间的可能关系，这些疾病包括β-淀粉样蛋白和tau蛋白，α-突触核蛋白和脱髓鞘。尚未完全阐明肥大症可能与各种神经退行性疾病的发病机理有关的机制。需要进一步的实验和临床研究来阐明关于肥大症​​在神经退行性疾病发病机理中潜在作用的假说。特别注意细胞铁过载与某些神经退行性疾病的关键病理特征之间的可能关系，这些疾病包括β-淀粉样蛋白和tau蛋白，α-突触核蛋白和脱髓鞘。尚未完全阐明肥大症可能与各种神经退行性疾病的发病机理有关的机制。需要进一步的实验和临床研究来阐明关于肥大症​​在神经退行性疾病发病机理中潜在作用的假说。特别注意细胞铁过载与某些神经退行性疾病的关键病理特征之间的可能关系，这些疾病包括β-淀粉样蛋白和tau蛋白，α-突触核蛋白和脱髓鞘。尚未完全阐明肥大症可能与各种神经退行性疾病的发病机理有关的机制。需要进一步的实验和临床研究来阐明关于肥大症​​在神经退行性疾病发病机理中潜在作用的假说。