线粒体
线粒体融合
线粒体分裂
多细胞生物
疾病
氧化应激
神经科学
生物
细胞凋亡
神经退行性变
线粒体通透性转换孔
细胞生物学
生物信息学
程序性细胞死亡
细胞
医学
线粒体DNA
遗传学
基因
病理
生物化学
作者
Ashish Dhiman,Mayank Handa,Munindra Ruwali,Dhirendra Singh,Prashant Kesharwani,Rahul Shukla
出处
期刊:Mitochondrion
[Elsevier]
日期:2022-05-01
卷期号:64: 112-124
被引量:7
标识
DOI:10.1016/j.mito.2022.03.006
摘要
Alzheimer's disease (AD) is the most ubiquitous neurodegenerative disorder with impaired cognitive functionality. Till date, the specific pathophysiology related to AD is still elusive. Recent reports suggest mitochondrial dysfunctionality like oxidative stress, Ca2+ disbalance, apoptosis, decrease energy and its metabolism plays an important. Recent reports about mitochondrial mechanisms and dynamics in AD unravelled new insights of molecular targets. Targeting multi-pathway via natural products may attenuate and prevent the mitochondria dysfunctionality. In this review, we have focused on the pathophysiology events of mitochondrial dysfunction in AD as well as mitochondrial fusion and fission mechanisms, role of aging in multicellular organisms, and how these connect to cell cycle regulation, and transmission of energy status.
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