Mitochondrial dysfunction plays a very vital role in the pathogenesis of Alzheimer’s disease (AD). Several shreds of evidence have indicated that the mitochondrial function is severely compromised under AD pathogenesis. Most of the recent therapeutic strategies have been conversed to treat AD by pinpointing the pathways involved in the pathophysiology of AD. In AD, mitochondria progressively lose their proper functions that are ultimately responsible for their accumulation and removal via the autophagic process, which is called mitophagy that further worsens the progression of this incapacitating disease. Preclinical and clinical studies have suggested that mitochondrial dysfunction along with mitophagy significantly contributes to the accumulation of amyloid-beta (Aβ) fibrils and hyperphosphorylated tau protein tangles which lead to synaptic dysfunctions and cognitive impairments such as memory loss through reactive oxygen species (ROS)–mediated pathway. The present review is intended to discuss the recent advancements in the frontiers of mitochondrial dysfunction and consequent therapeutic strategies that have been employed to treat AD.

线粒体功能障碍在阿尔茨海默氏病（AD）的发病机理中起着至关重要的作用。几类证据表明，AD发病机制下线粒体功能严重受损。通过查明与AD病理生理学有关的途径，将大多数最近的治疗策略进行了逆转。在AD中，线粒体逐渐丧失其正常功能，这些功能最终通过自噬过程导致其积累和去除，这被称为线粒体吞噬，这进一步加剧了这种无行为能力的疾病的发展。临床前和临床研究表明，线粒体功能障碍和线粒体吞噬显着促进了β-淀粉样蛋白（Aβ）纤维和磷酸化tau蛋白缠结的积累，从而导致突触功能障碍和认知障碍，例如通过活性氧（ROS）导致的记忆力减退–介导的途径。本综述旨在讨论线粒体功能障碍前沿的最新进展以及已被用于治疗AD的治疗策略。