线粒体
疾病
神经科学
线粒体生物发生
生物
线粒体融合
细胞色素c氧化酶
阿尔茨海默病
MFN1型
表型
内表型
神经退行性变
人口
医学
线粒体DNA
认知
病理
细胞生物学
遗传学
基因
环境卫生
作者
J. Eva Selfridge,E Lezi,Jianghua Lu,Russell H. Swerdlow
标识
DOI:10.1016/j.nbd.2011.12.057
摘要
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.
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