Stimulation of electron transport as potential novel therapy in Parkinson's disease with mitochondrial dysfunction

被引:8
作者
Vos, Melissa [1 ,2 ,3 ,4 ]
Verstreken, Patrik [2 ,3 ,4 ]
Klein, Christine [1 ]
机构
[1] Med Univ Lubeck, Inst Neurogenet, D-23538 Lubeck, Germany
[2] VIB Ctr Biol Dis, Leuven, Belgium
[3] Katholieke Univ Leuven, Dept Human Genet, Leuven, Belgium
[4] Katholieke Univ Leuven, Leuven Res Inst Neurosci & Dis LIND, Leuven, Belgium
基金
欧洲研究理事会;
关键词
electron transport chain; mitochondria; Parkinson's disease; Pink1; vitamin K-2; RANDOMIZED CLINICAL-TRIAL; EARLY-ONSET PARKINSONISM; COMPLEX I ACTIVITY; RESPIRATORY-CHAIN; SKELETAL-MUSCLE; DOPAMINERGIC-NEURONS; COENZYME Q(10); DOUBLE-BLIND; PINK1; MUTATIONS;
D O I
10.1042/BST20140325
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Parkinson's disease (PD) is a neurodegenerative motor disorder characterized by the loss of dopaminergic neurons. This loss of dopaminergic neurons is the pathological hallmark of the disease that results in the characteristic motor syndrome. Restoration of dopamine levels is the basis of current therapy; however, this does not tackle the cause of the disease. While the aetiology of PD remains mostly elusive, mitochondrial dysfunction has been linked to (at least) part of the PD cases. In this review we discuss recent findings in Drosophila melanogaster showing that stimulation of the electron transport chain is beneficial for PD fly models showing Complex I defects and discuss the possible clinical applications of these findings.
引用
收藏
页码:275 / 279
页数:5
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