Large Animal Diagnostic Laboratory, Department of Clinical Veterinary Medicine, Ethics & Jurisprudence, Division of Veterinary Biochemistry, Faculty of Veterinary Sciences and Animal Husbandry, Sher-e-Kashmir University of Agricultural Sciences and Technology (SKUAST-K), Srinagar J&K-190006, India.
Department of Pharmacology and Toxicology, College of Pharmacy, Jazan University, Jazan, 45142, Saudi Arabia.
Oxid Med Cell Longev. 2022 May 14;2022:4759963. doi: 10.1155/2022/4759963. eCollection 2022.
Mitochondria play a critical role in neuron viability or death as it regulates energy metabolism and cell death pathways. They are essential for cellular energy metabolism, reactive oxygen species production, apoptosis, Ca homeostasis, aging, and regeneration. Mitophagy and mitochondrial dynamics are thus essential processes in the quality control of mitochondria. Improvements in several fundamental features of mitochondrial biology in susceptible neurons of AD brains and the putative underlying mechanisms of such changes have made significant progress. AD's etiology has been reported by mitochondrial malfunction and oxidative damage. According to several recent articles, a continual fusion and fission balance of mitochondria is vital in their normal function maintenance. As a result, the shape and function of mitochondria are inextricably linked. This study examines evidence suggesting that mitochondrial dysfunction plays a significant early impact on AD pathology. Furthermore, the dynamics and roles of mitochondria are discussed with the link between mitochondrial malfunction and autophagy in AD has also been explored. In addition, recent research on mitochondrial dynamics and mitophagy in AD is also discussed in this review. It also goes into how these flaws affect mitochondrial quality control. Furthermore, advanced therapy techniques and lifestyle adjustments that lead to improved management of the dynamics have been demonstrated, hence improving the conditions that contribute to mitochondrial dysfunction in AD.
线粒体在神经元的存活或死亡中起着至关重要的作用，因为它调节能量代谢和细胞死亡途径。线粒体对于细胞能量代谢、活性氧物种的产生、细胞凋亡、钙稳态、衰老和再生都是必不可少的。因此，线粒体自噬和线粒体动力学是线粒体质量控制的必要过程。AD 大脑中易感神经元中线粒体生物学的几个基本特征的改善以及这些变化的潜在机制已经取得了重大进展。线粒体功能障碍和氧化损伤被报道是 AD 的病因。根据最近的一些研究，线粒体的持续融合和裂变平衡对于维持其正常功能至关重要。因此，线粒体的形状和功能是紧密相连的。本研究探讨了线粒体功能障碍在 AD 病理中的早期显著影响的证据。此外，还讨论了线粒体的动态和作用，以及 AD 中线粒体功能障碍与自噬之间的联系。此外，本文还讨论了 AD 中关于线粒体动力学和线粒体自噬的最新研究。它还研究了这些缺陷如何影响线粒体的质量控制。此外，还展示了如何通过先进的治疗技术和生活方式的调整来改善对动态的管理，从而改善导致 AD 中线粒体功能障碍的条件。
