突触囊泡循环障碍与帕金森病

Dysfunction of synaptic vesicle recycling and Parkinson's disease

帕金森病是人类第二大神经退行性疾病,虽然通过对帕金森病遗传家族的研究已发现不少与之相关的致病基因,然而其病因尚不清楚。在已发现的与帕金森病相关基因中,α-synuclein、LRRK2、Parkin、PINK1以及DJ-1也在调节神经元突触前囊泡的神经递质释放以及突触前囊泡循环过程中发挥重要作用。最近的一些研究表明突触前囊泡循环障碍在帕金森病发病过程中扮演重要角色。本文对上述基因在突触囊泡循环以及其突变导致帕金森病病程中的作用作一概述,并推测囊泡循环障碍在帕金森病发病过程中的作用机理,最后指出目前在该研究领域需要解决的一些问题。

The etiology of Parkinson＇s disease （PD） remains unclear, despite a large number of genes linked to this neurodegenerative disorder. Many of the genes related to PD such as α-synuclein, LRRK2, Parkin, PINK1, and D J-1 encode proteins that play key roles in regulation of neurotransmitter release from synaptic vesicle and vesicle recycling. Recent studies have suggested that the dysfunction of synaptic vesicle recycling at presynaptic terminals may contribute to the onset of PD. Here we review the functions of α-synuclein, LRRK2, Parkin, P1NK1, and D J-1 in synaptic vesicle recycling during synaptic transmission and discuss how synaptic dysfunction may contribute to the progression of Parkinson＇s disease.