Department of Molecular and Integrative Physiology, University of Kansas School of Medicine, Kansas City, KS 66160, USA.
Neurobiol Dis. 2013 Mar;51:3-12. doi: 10.1016/j.nbd.2011.12.057. Epub 2012 Jan 10.
Alzheimer's disease (AD) is a progressive neurodegenerative disease that affects a staggering percentage of the aging population and causes memory loss and cognitive decline. Mitochondrial abnormalities can be observed systemically and in brains of patients suffering from AD, and may account for part of the disease phenotype. In this review, we summarize some of the key findings that indicate mitochondrial dysfunction is present in AD-affected subjects, including cytochrome oxidase deficiency, endophenotype data, and altered mitochondrial morphology. Special attention is given to recently described perturbations in mitochondrial autophagy, fission-fusion dynamics, and biogenesis. We also briefly discuss how mitochondrial dysfunction may influence amyloidosis in Alzheimer's disease, why mitochondria are a valid therapeutic target, and strategies for addressing AD-specific mitochondrial dysfunction.
阿尔茨海默病（AD）是一种进行性神经退行性疾病，影响着庞大的老年人群体，导致记忆丧失和认知能力下降。在患有 AD 的患者的全身和大脑中都可以观察到线粒体异常，这可能是部分疾病表型的原因。在这篇综述中，我们总结了一些关键发现，表明 AD 患者存在线粒体功能障碍，包括细胞色素氧化酶缺乏、内表型数据和线粒体形态改变。特别关注最近描述的线粒体自噬、裂变融合动力学和生物发生的扰动。我们还简要讨论了线粒体功能障碍如何影响阿尔茨海默病中的淀粉样蛋白沉积、为什么线粒体是一个有效的治疗靶点以及解决 AD 特异性线粒体功能障碍的策略。
