线粒体功能障碍与神经退行性疾病:病因还是后果?

Mitochondria dysfunction and neurodegenerative disorders: cause or consequence.

机构信息

Center for Human Genetics, K.U. Leuven, Belgium.

出版信息

J Alzheimers Dis. 2010;20 Suppl 2:S255-63. doi: 10.3233/JAD-2010-100345.

Abstract

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.

摘要

线粒体是能量代谢和凋亡途径的关键调节因子,与神经退行性疾病的发病机制密切相关。在这篇综述中,我们主要关注两种最常见的神经退行性疾病:阿尔茨海默病和帕金森病中的线粒体功能障碍。我们讨论了线粒体在这些疾病中的作用是应该被认为是原发性的,还是应该被认为是继发于其他最终导致神经退行性变的过程。就帕金森病而言,线粒体的作用相当明确,可能参与了这种疾病的发病机制。对于阿尔茨海默病,支持这种联系的证据更为间接,线粒体功能障碍可能发生在疾病的后期。

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