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The Evolution-Driven Signature of Parkinson’s Disease
Trends in Neurosciences ( IF 15.9 ) Pub Date : 2020-07-01 , DOI: 10.1016/j.tins.2020.05.001
Nico J Diederich 1 , Toshiki Uchihara 2 , Sten Grillner 3 , Christopher G Goetz 4
Affiliation  

In this review, we approach Parkinson's disease (PD) in the context of an evolutionary mismatch of central nervous system functions. The neurons at risk have hyperbranched axons, extensive transmitter release sites, display spontaneous spiking, and elevated mitochondrial stress. They function in networks largely unchanged throughout vertebrate evolution, but now connecting to the expanded human cortex. Their breakdown is favoured by longevity. At the cellular level, mitochondrial dysfunction starts at the synapses, then involves axons and cell bodies. At the behavioural level, network dysfunctions provoke the core motor syndrome of parkinsonism including freezing and failed gait automatization, and non-motor deficits including inactive blindsight and autonomic dysregulation. The proposed evolutionary re-interpretation of PD-prone cellular phenotypes and of prototypical clinical symptoms allows a new conceptual framework for future research.

中文翻译:

帕金森病的进化驱动特征

在这篇综述中,我们在中枢神经系统功能进化不匹配的背景下处理帕金森病 (PD)。处于危险中的神经元具有高度分支的轴突、广泛的递质释放位点、显示出自发的尖峰信号和升高的线粒体压力。它们在整个脊椎动物进化过程中在网络中的功能基本保持不变,但现在连接到扩展的人类皮层。他们的崩溃受到长寿的青睐。在细胞水平上,线粒体功能障碍始于突触,然后涉及轴突和细胞体。在行为层面,网络功能障碍会引发帕金森病的核心运动综合征,包括冻结和步态自动化失败,以及非运动缺陷,包括非活动性盲视和自主神经失调。
更新日期:2020-07-01
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