发病机制
帕金森病
疾病
线粒体
病毒学
医学
生物
免疫学
神经科学
细胞生物学
病理
作者
Gaia Faustini,Federica Bono,Alessandra Valerio,Marina Pizzi,PierFranco Spano,Arianna Bellucci
出处
期刊:Genes
[MDPI AG]
日期:2017-12-08
卷期号:8 (12): 377-377
被引量:45
摘要
Parkinson's disease (PD) is a movement disorder characterized by dopaminergic nigrostriatal neuron degeneration and the formation of Lewy bodies (LB), pathological inclusions containing fibrils that are mainly composed of α-synuclein. Dopaminergic neurons, for their intrinsic characteristics, have a high energy demand that relies on the efficiency of the mitochondria respiratory chain. Dysregulations of mitochondria, deriving from alterations of complex I protein or oxidative DNA damage, change the trafficking, size and morphology of these organelles. Of note, these mitochondrial bioenergetics defects have been related to PD. A series of experimental evidence supports that α-synuclein physiological action is relevant for mitochondrial homeostasis, while its pathological aggregation can negatively impinge on mitochondrial function. It thus appears that imbalances in the equilibrium between the reciprocal modulatory action of mitochondria and α-synuclein can contribute to PD onset by inducing neuronal impairment. This review will try to highlight the role of physiological and pathological α-synuclein in the modulation of mitochondrial functions.
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