粒体自噬
神经科学
线粒体
氧化应激
疾病
线粒体融合
认知
机制(生物学)
医学
认知功能衰退
生物信息学
生物
病理
细胞生物学
痴呆
线粒体DNA
自噬
内分泌学
物理
细胞凋亡
生物化学
量子力学
基因
作者
You Wang,Yue Li,Kaixi Liu,Xinning Mi,Yitong Li,Xiangyang Guo,Zhengqian Li
标识
DOI:10.4103/1673-5374.382222
摘要
Mitochondria play an essential role in neural function, such as supporting normal energy metabolism, regulating reactive oxygen species, buffering physiological calcium loads, and maintaining the balance of morphology, subcellular distribution, and overall health through mitochondrial dynamics. Given the recent technological advances in the assessment of mitochondrial structure and functions, mitochondrial dysfunction has been regarded as the early and key pathophysiological mechanism of cognitive disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, mild cognitive impairment, and postoperative cognitive dysfunction. This review will focus on the recent advances in mitochondrial medicine and research methodology in the field of cognitive sciences, from the perspectives of energy metabolism, oxidative stress, calcium homeostasis, and mitochondrial dynamics (including fission-fusion, transport, and mitophagy).
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