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首页> 外文期刊>Biological communications >Malfunctions in synaptic membrane trafficking in early pathology of Parkinson's disease: New molecular clues
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Malfunctions in synaptic membrane trafficking in early pathology of Parkinson's disease: New molecular clues

机译：故障在突触膜贩运帕金森病的早期病理:新的分子的线索

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摘要

The midbrain dopaminergic neurons of the substantia nigra and the ventral tegmental area play vital roles in the regulation of voluntary movement, emotion and reward in humans. These neurons are highly metabolic and are under constant oxidative stress. The dopaminergic neurons form extensive synaptic projections to the striatum. When these neurons start dying or when their synaptic connections fail, humans develop Parkinson? disease. This disease is accompanied by the accumulation of toxic α-synuclein-containing protein aggregates in nigrostriatal processes. Synucleins accumulate in a majority of healthy nerve terminals in the central nervous system, but what causes the formation of pathological synuclein aggregates is unclear. Recent studies point out that the interface between membrane trafficking in the nerve terminal and the autophagy- lysosomal pathway is the site for the aggregate assembly. An urgent goal is to find therapeutic targets at early stages of the disease when neurons are still functional.
机译：中脑多巴胺能神经元的黑质和腹侧被盖区在其中扮演重要角色的监管自愿的运动,在人类情感和奖励。神经元是高代谢和以下持续的氧化应激。广泛神经元形成突触的预测纹状体。当他们的突触连接失败,人类发展帕金森?伴随着有毒的积累α-synuclein-containing蛋白质聚合黑的过程。大多数健康的神经终端中枢神经系统,但是是什么原因导致的形成的病理-核蛋白聚集不清楚。界面膜贩运之间神经终端和自噬-溶酶体通路的网站总装配。迫切的目标是找到治疗目标当神经元疾病的早期阶段还是功能。

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