粒体自噬
线粒体生物发生
神经保护
疾病
神经科学
线粒体
阿尔茨海默病
衰老的大脑
医学
生物
生物信息学
认知
自噬
细胞生物学
内科学
遗传学
细胞凋亡
作者
Lili Feng,Bowen Li,Su Yong,Wen Xu,Zhenjun Tian
标识
DOI:10.1016/j.arr.2024.102486
摘要
Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by memory impairment and cognitive dysfunction, which eventually leads to the disability and mortality of older adults. Although the precise mechanisms by which age promotes the development of AD remains poorly understood, mitochondrial dysfunction plays a central role in the development of AD. Currently, there is no effective treatment for this debilitating disease. It is well accepted that exercise exerts neuroprotective effects by ameliorating mitochondrial dysfunction in the neurons of AD, which involves multiple mechanisms, including mitochondrial dynamics, biogenesis, mitophagy, transport, and signal transduction. In addition, exercise promotes mitochondria communication with other organelles in AD neurons, which should receive more attentions in the future.
科研通智能强力驱动
Strongly Powered by AbleSci AI