Abnormally high brain iron, resulting from the disrupted expression or function of proteins involved in iron metabolism in the brain, is an initial cause of neuronal death in neuroferritinopathy and aceruloplasminemia, and also plays a causative role in at least some of the other neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and Friedreich's ataxia. As such, iron is believed to be a novel target for pharmacological intervention in these disorders. Reducing iron toward normal levels or hampering the increases in iron associated with age in the brain is a promising therapeutic strategy for all iron‐related neurodegenerative disorders. Hepcidin is a crucial regulator of iron homeostasis in the brain. Recent studies have suggested that upregulating brain hepcidin levels can significantly reduce brain iron content through the regulation of iron transport protein expression in the blood‐brain barrier and in neurons and astrocytes. In this review, we focus on the discussion of the therapeutic potential of hepcidin in iron‐associated neurodegenerative diseases and also provide a systematic overview of recent research progress on how misregulated brain iron metabolism is involved in the development of multiple neurodegenerative disorders.

中文翻译：

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铁调素及其在神经退行性疾病中的治疗潜力。

脑铁代谢异常涉及蛋白质的表达或功能异常，导致脑铁异常高位，是神经铁蛋白病和铜蓝蛋白血症的神经元死亡的最初原因，并且在至少一些其他神经退行性疾病中也起着致病作用阿尔茨海默氏病，帕金森氏病，亨廷顿氏病和弗里德里希共济失调。因此，铁被认为是这些疾病中药理干预的新靶标。将铁降低至正常水平或阻止与年龄相关的铁的增加是所有与铁相关的神经退行性疾病的有前途的治疗策略。铁调素是大脑中铁稳态的关键调节剂。最近的研究表明，通过调节血脑屏障以及神经元和星形胶质细胞中铁转运蛋白的表达，上调脑铁素水平可以显着降低脑铁含量。在这篇综述中，我们着重讨论铁调素在铁相关的神经退行性疾病中的治疗潜力，并提供系统的综述，综述了关于脑铁代谢失调如何参与多种神经退行性疾病发展的最新研究进展。