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帕金森病相关的线粒体功能障碍的小鼠模型。

Mouse models of Parkinson's disease associated with mitochondrial dysfunction.

机构信息

Neuroscience Graduate Program, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.

出版信息

Mol Cell Neurosci. 2013 Jul;55:87-94. doi: 10.1016/j.mcn.2012.08.002. Epub 2012 Aug 11.

DOI:10.1016/j.mcn.2012.08.002
PMID:22954895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3997253/
Abstract

Despite years of intensive research, the understanding of Parkinson's disease (PD) is still rudimentary. Genetic causes of rare familial cases have offered venues of investigation, and interestingly, have strengthened the case for a mitochondrial dysfunction in the pathogenesis of PD. Mouse models, where these and other mitochondrial-related genes are affected are helping not only in understanding PD, but also in providing a powerful tool to test therapeutics. In this review, we will discuss the different characteristics of these mouse models. This article is part of a Special Issue entitled 'Mitochondrial function and dysfunction in neurodegeneration'.

摘要

尽管经过多年的深入研究,人们对帕金森病 (PD) 的认识仍然很基础。罕见家族性病例的遗传原因提供了研究的途径,有趣的是,这也加强了线粒体功能障碍在 PD 发病机制中的作用。受这些和其他与线粒体相关基因影响的小鼠模型不仅有助于了解 PD,而且为测试治疗方法提供了有力工具。在这篇综述中,我们将讨论这些小鼠模型的不同特征。本文是特刊“神经退行性疾病中的线粒体功能和功能障碍”的一部分。

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本文引用的文献

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Conditional expression of Parkinson's disease-related mutant α-synuclein in the midbrain dopaminergic neurons causes progressive neurodegeneration and degradation of transcription factor nuclear receptor related 1.帕金森病相关突变型α-突触核蛋白在中脑多巴胺能神经元中的条件性表达导致进行性神经退行性变和转录因子核受体相关 1 的降解。
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Parkinson's disease-associated kinase PINK1 regulates Miro protein level and axonal transport of mitochondria.帕金森病相关激酶 PINK1 调节 Miro 蛋白水平和线粒体的轴突运输。
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单侧纹状体注射肉毒毒素 A 对 C57BL/6 小鼠和大鼠的运动行为影响不同。
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Inhibition of neuronal cell mitochondrial complex I with rotenone increases lipid β-oxidation, supporting acetyl-coenzyme A levels.用鱼藤酮抑制神经元细胞线粒体复合物I可增加脂质β-氧化,维持乙酰辅酶A水平。
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LRRK2 regulates mitochondrial dynamics and function through direct interaction with DLP1.LRRK2 通过与 DLP1 的直接相互作用调节线粒体动力学和功能。
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