Smt. Kishoritai Bhoyar College of Pharmacy, Kamptee 441002, Maharashtra, India.
SNJB's Shriman Sureshdada Jain College of Pharmacy, Neminagar, Chandawad 423101, Maharashtra, India.
Curr Pharm Des. 2024;30(12):902-911. doi: 10.2174/0113816128286655240304070740.
Neurodegenerative disorders are distinguished by the progressive loss of anatomically or physiologically relevant neural systems. Atypical mitochondrial morphology and metabolic malfunction are found in many neurodegenerative disorders. Alteration in mitochondrial function can occur as a result of aberrant mitochondrial DNA, altered nuclear enzymes that interact with mitochondria actively or passively, or due to unexplained reasons. Mitochondria are intimately linked to the Endoplasmic reticulum (ER), and ER-mitochondrial communication governs several of the physiological functions and procedures that are disrupted in neurodegenerative disorders. Numerous researchers have associated these disorders with ER-mitochondrial interaction disturbance. In addition, aberrant mitochondrial DNA mutation and increased ROS production resulting in ionic imbalance and leading to functional and structural alterations in the brain as well as cellular damage may have an essential role in disease progression via mitochondrial malfunction. In this review, we explored the evidence highlighting the role of mitochondrial alterations in neurodegenerative pathways in most serious ailments, including Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD).
神经退行性疾病的特征是解剖学或生理学上相关的神经网络进行性丧失。许多神经退行性疾病中存在异常的线粒体形态和代谢功能障碍。线粒体功能的改变可能是由于异常的线粒体 DNA、主动或被动与线粒体相互作用的核酶改变,或由于未知原因引起的。线粒体与内质网(ER)密切相关,ER-线粒体通讯调控着几种在神经退行性疾病中被破坏的生理功能和过程。许多研究人员将这些疾病与 ER-线粒体相互作用障碍联系起来。此外,异常的线粒体 DNA 突变和 ROS 产生增加导致离子失衡,导致大脑的功能和结构改变以及细胞损伤,可能通过线粒体功能障碍在疾病进展中起关键作用。在这篇综述中,我们探讨了强调线粒体改变在包括阿尔茨海默病(AD)、帕金森病(PD)和亨廷顿病(HD)在内的大多数严重疾病的神经退行性途径中的作用的证据。