Alpha-Synuclein and Mitochondrial Dysfunction in Parkinson’s Disease

被引：4
作者：
Dolgacheva L.P. [1 ]
Fedotova E.I. [1 ]
Abramov A.Y. [2 ]
Berezhnov A.V. [1 ]
机构：
[1] Istitute of Cell Biophysics of Russian Academy of Sciences, Pushchino, Moscow oblast
[2] Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London
来源：
Biochemistry (Moscow), Supplement Series A: Membrane and Cell Biology | 2018年 / 12卷 / 1期
基金：
俄罗斯基础研究基金会;
关键词：
alpha-synuclein; mitochondria; neurodegeneration; Parkinson’s disease;
D O I：
10.1134/S1990747818010038
中图分类号：
学科分类号：
摘要：
Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. The development of pathology is associated with the loss of dopaminergic neurons, mainly in substantia nigra pars compacta. Dopamine deficiency causes a whole range of severe motor symptoms, including bradykinesia, postural instability, muscle rigidity, and tremor. Studies have shown the primary role of the alpha-synuclein protein in this neurodegenerative disease. A large amount of data indicates different mechanisms of the toxic effect of alpha-synuclein. The process of neurodegeneration in PD is the result of significant disturbances in mitochondrial functions and/or genetic mutations. The number of mutated genes in hereditary and sporadic forms of Parkinson’s disease includes genes encoding PINK1 and Parkin, which are the main participants in the mitochondrial “quality control” system. The earliest biochemical hallmarks of the disease are disturbances of the mitochondrial interaction with endoplasmic reticulum, mitochondrial dynamics, Ca2+ homeostasis, and an increase in the level of mitochondrial reactive oxygen species. All these factors exert damaging effects on dopaminergic neurons. © 2018, Pleiades Publishing, Ltd.
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页码：10 / 19
页数：9
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