Mitochondria Dysfunction and Neurodegenerative Disorders: Cause or Consequence

被引:91
|
作者
Morais, Vanessa A. [1 ,2 ]
De Strooper, Bart [2 ]
机构
[1] Katholieke Univ Leuven VIB, Dept Mol & Dev Genet, Lab Res Neurodegenerat Dis, B-3000 Louvain, Belgium
[2] Katholieke Univ Leuven, Ctr Human Genet, Louvain, Belgium
关键词
Alzheimer's disease; apoptosis; mitochondria; oxidative stress; Parkinson's disease; AMYLOID-BETA-PEPTIDE; DROSOPHILA-PARKIN MUTANTS; ALZHEIMERS-DISEASE; ALPHA-SYNUCLEIN; A-BETA; COMPLEX-I; OXIDATIVE DAMAGE; PC12; CELLS; RECESSIVE PARKINSONISM; INCREASED SENSITIVITY;
D O I
10.3233/JAD-2010-100345
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Mitochondria are crucial regulators of energy metabolism and apoptotic pathways and have been closely linked to the pathogenesis of neurodegenerative disorders. In this review we mainly focus on mitochondrial dysfunction in two of the most prevalent neurological disorders: Alzheimer's disease and Parkinson's disease. We discuss whether the role of mitochondria in those diseases should be considered primordial or secondary to other processes that eventually lead to neurodegeneration. In the case of Parkinson's disease, the role of mitochondria is quite clear and might be involved in the mechanism of this disorder. For Alzheimer's disease, the evidence in favor of such a link is more indirect, and mitochondrial dysfunction likely occurs at a later stage of the disorder.
引用
收藏
页码:S255 / S263
页数:9
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