Cai Qian, Tammineni Prasad
Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey Piscataway, NJ, USA.
Front Cell Neurosci. 2016 Feb 9;10:24. doi: 10.3389/fncel.2016.00024. eCollection 2016.
Mitochondrial dysfunction is one of the earliest and most prominent features in the brains of Alzheimer's disease (AD) patients. Recent studies suggest that mitochondrial dysfunction plays a pivotal role in the pathogenesis of AD. Neurons are metabolically active cells, causing them to be particularly dependent on mitochondrial function for survival and maintenance. As highly dynamic organelles, mitochondria are characterized by a balance of fusion and fission, transport, and mitophagy, all of which are essential for maintaining mitochondrial integrity and function. Mitochondrial dynamics and mitophagy can therefore be identified as key pathways in mitochondrial quality control. Tremendous progress has been made in studying changes in these key aspects of mitochondrial biology in the vulnerable neurons of AD brains and mouse models, and the potential underlying mechanisms of such changes. This review highlights recent findings on alterations in the mitochondrial dynamics and mitophagy in AD and discusses how these abnormalities impact mitochondrial quality control and thus contribute to mitochondrial dysfunction in AD.
线粒体功能障碍是阿尔茨海默病（AD）患者大脑中最早出现且最为突出的特征之一。最近的研究表明，线粒体功能障碍在AD的发病机制中起关键作用。神经元是代谢活跃的细胞，这使得它们在生存和维持过程中特别依赖线粒体功能。作为高度动态的细胞器，线粒体的特征在于融合与裂变、运输以及线粒体自噬之间的平衡，所有这些对于维持线粒体的完整性和功能都至关重要。因此，线粒体动力学和线粒体自噬可被视为线粒体质量控制的关键途径。在研究AD大脑和小鼠模型中易损神经元中线粒体生物学这些关键方面的变化及其潜在机制方面已经取得了巨大进展。本综述重点介绍了AD中线粒体动力学和线粒体自噬改变的最新发现，并讨论了这些异常如何影响线粒体质量控制，进而导致AD中的线粒体功能障碍。
