致密黑质神经元的特异性易感性。

Marten P Smidt
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引用次数: 4

摘要

帕金森病(PD)中致密黑质(SNc)神经元的特异性缺失一直是启动SNc特异性脆弱性研究的主要动力。最初,由于高多巴胺周转率引起的代谢限制一直是试图解决这一问题的主要焦点。最近,分子特征的根本差异增加了神经元的脆弱性,并提供了特定的分子依赖性,这一点已经变得很清楚。本文总结了定义SNc脆弱性分子背景的不同过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Specific vulnerability of substantia nigra compacta neurons.

The specific loss of substantia nigra compacta (SNc) neurons in Parkinson's disease (PD) has been the main driving force in initiating research efforts to unravel the apparent SNc-specific vulnerability. Initially, metabolic constraints due to high dopamine turnover have been the main focus in the attempts to solve this issue. Recently, it has become clear that fundamental differences in the molecular signature are adding to the neuronal vulnerability and provide specific molecular dependencies. Here, the different processes that define the molecular background of SNc vulnerability are summarized.

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