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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Nexus between mitochondrial function, iron, copper and glutathione in Parkinson's disease
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Nexus between mitochondrial function, iron, copper and glutathione in Parkinson's disease

机译：帕金森病的线粒体功能，铁，铜和谷胱甘肽之间的Nexus

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摘要

Parkinson's disease is neuropathologically characterised by loss of catecholamine neurons in vulnerable brain regions including substantia nigra pars compacta and locus coeruleus. This review discusses how the susceptibility of these regions is defined by their shared biochemical characteristics that differentiate them from other neurons. Parkinson's disease is biochemically characterised by mitochondrial dysfunction, accumulation of iron, diminished copper content and depleted glutathione levels in these regions. This review also discusses this neuropathology, and provides evidence for how these pathological features are mechanistically linked to each other. This leads to the conclusion that disruption of mitochondrial function, or iron, copper or glutathione metabolism in isolation provokes the pathological impairment of them all. This creates a vicious cycle that drives pathology leading to mitochondrial failure and neuronal cell death in vulnerable brain regions. (C) 2017 Elsevier Ltd. All rights reserved.
机译：帕金森病是神经病理学，其特征在于脆弱的脑地区的儿茶酚胺神经元，包括Complia Nigra Compara和Locus Coeruleus。本综述讨论了这些区域的易感性如何由其共同的生化特征来定义，这些特征将它们与其他神经元区分开来。帕金森病的疾病是通过线粒体功能障碍，铁的积累，铜含量减少和贫肠道水平在这些地区的疾病。该审查还讨论了这种神经病理学，并提供了这些病理特征如何彼此机械化的证据。这导致了孤立中断线粒体功能，或铁，铜或谷胱甘肽代谢的干扰引起了他们所有人的病理障碍。这产生了一种恶性循环，推动病理学导致脆弱的脑区中的线粒体失效和神经细胞死亡。 （c）2017 Elsevier Ltd.保留所有权利。

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