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铁与神经退行性变:从细胞内稳态到疾病。

Iron and neurodegeneration: from cellular homeostasis to disease.

机构信息

Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, EAN, Oeiras, Portugal.

出版信息

Oxid Med Cell Longev. 2012;2012:128647. doi: 10.1155/2012/128647. Epub 2012 May 30.

DOI:10.1155/2012/128647
PMID:22701145
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3369498/
Abstract

Accumulation of iron (Fe) is often detected in the brains of people suffering from neurodegenerative diseases. High Fe concentrations have been consistently observed in Parkinson's, Alzheimer's, and Huntington's diseases; however, it is not clear whether this Fe contributes to the progression of these diseases. Other conditions, such as Friedreich's ataxia or neuroferritinopathy are associated with genetic factors that cause Fe misregulation. Consequently, excessive intracellular Fe increases oxidative stress, which leads to neuronal dysfunction and death. The characterization of the mechanisms involved in the misregulation of Fe in the brain is crucial to understand the pathology of the neurodegenerative disorders and develop new therapeutic strategies. Saccharomyces cerevisiae, as the best understood eukaryotic organism, has already begun to play a role in the neurological disorders; thus it could perhaps become a valuable tool also to study the metalloneurobiology.

摘要

在患有神经退行性疾病的人的大脑中经常检测到铁 (Fe) 的积累。在帕金森病、阿尔茨海默病和亨廷顿病中一直观察到高浓度的 Fe;然而,尚不清楚这种 Fe 是否有助于这些疾病的进展。其他疾病,如弗里德里希共济失调或神经铁蛋白病,与导致 Fe 失调的遗传因素有关。因此,过多的细胞内 Fe 会增加氧化应激,从而导致神经元功能障碍和死亡。阐明脑内 Fe 失调的机制对于理解神经退行性疾病的病理学和开发新的治疗策略至关重要。酿酒酵母作为最被理解的真核生物,已经开始在神经紊乱中发挥作用;因此,它也可能成为研究金属神经生物学的有用工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a89/3369498/9759143b1e8e/OXIMED2012-128647.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a89/3369498/9759143b1e8e/OXIMED2012-128647.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a89/3369498/9759143b1e8e/OXIMED2012-128647.001.jpg

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