粒体自噬
线粒体
神经科学
细胞生物学
神经退行性变
生物
程序性细胞死亡
氧化应激
氧化磷酸化
疾病
机制(生物学)
自噬
医学
细胞凋亡
病理
生物化学
认识论
哲学
作者
Jangampalli Adi Pradeepkiran,Javaria Baig,Ashley Selman,P. Hemachandra Reddy
出处
期刊:The Neuroscientist
[SAGE]
日期:2023-01-03
卷期号:: 107385842211397-107385842211397
被引量:13
标识
DOI:10.1177/10738584221139761
摘要
Alzheimer’s disease (AD) is characterized by the accumulation of amyloid β and phosphorylated τ protein aggregates in the brain, which leads to the loss of neurons. Under the microscope, the function of mitochondria is uniquely primed to play a pivotal role in neuronal cell survival, energy metabolism, and cell death. Research studies indicate that mitochondrial dysfunction, excessive oxidative damage, and defective mitophagy in neurons are early indicators of AD. This review article summarizes the latest development of mitochondria in AD: 1) disease mechanism pathways, 2) the importance of mitochondria in neuronal functions, 3) metabolic pathways and functions, 4) the link between mitochondrial dysfunction and mitophagy mechanisms in AD, and 5) the development of potential mitochondrial-targeted therapeutics and interventions to treat patients with AD.
科研通智能强力驱动
Strongly Powered by AbleSci AI