What lysosomes actually tell us about Parkinson's disease?

被引：21
作者：
Bourdenx, Mathieu [1 ,2 ]
Dehay, Benjamin [1 ,2 ]
机构：
[1] Univ Bordeaux, Inst Malad Neurodegenerat, UMR 5293, Bordeaux, France
[2] CNRS, Inst Malad Neurodegenerat, UMR 5293, Bordeaux, France
来源：
AGEING RESEARCH REVIEWS | 2016年 / 32卷
关键词：
Parkinson's disease; Lysosomes; Neurodegeneration; Therapeutic; CHAPERONE-MEDIATED AUTOPHAGY; PROTEIN-DEGRADATION PATHWAYS; MIDBRAIN DOPAMINE NEURONS; MUTANT ALPHA-SYNUCLEIN; LEWY BODY; IN-VIVO; GAUCHER-DISEASE; GBA MUTATIONS; CATHEPSIN-D; RISK-FACTOR;
D O I：
10.1016/j.arr.2016.02.008
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Parkinson's disease is a common neurodegenerative disorder of unknown origin mainly characterized by the loss of neuromelanin-containing dopaminergic neurons in the substantia nigra pars compacta and the presence of intraneuronal proteinaceous inclusions called Lewy bodies. Lysosomes are dynamic organelles that degrade, in a controlled manner, cellular components delivered via the secretory, endocytic, autophagic and phagocytic membrane-trafficking pathways. Increasing amounts of evidence suggest a central role of lysosomal impairment in PD aetiology. This review provides an update on how genetic evidence support this connection and highlights how the neuropathologic and mechanistic evidence might relate to the disease process in sporadic forms of Parkinson's disease. Finally, we discuss the influence of ageing on lysosomal impairment and PD aetiology and therapeutic strategies targeting lysosomal function. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码：140 / 149
页数：10
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