Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, 8 Baltiiskaya Street, 125315 Moscow, Russia.
Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 14-3 Solyanka Street, 109240 Moscow, Russia.
Int J Mol Sci. 2022 Jun 23;23(13):6954. doi: 10.3390/ijms23136954.
Mitochondrial dysfunction is now recognized as a contributing factor to neurodegenerative diseases, including Alzheimer's disease (AD). Mitochondria are signaling organelles with a variety of functions ranging from energy production to the regulation of cellular metabolism, energy homeostasis, and response to stress. The successful functioning of these complex processes is critically dependent on the accuracy of mitochondrial dynamics, which includes the ability of mitochondria to change shape and position in the cell, which is necessary to maintain proper function and quality control, especially in polarized cells such as neurons. There has been much evidence to suggest that the disruption of mitochondrial dynamics may play a critical role in the pathogenesis of AD. This review highlights aspects of altered mitochondrial dynamics in AD that may contribute to the etiology of this debilitating condition. We also discuss therapeutic strategies to improve mitochondrial dynamics and function that may provide an alternative treatment approach.
线粒体功能障碍现在被认为是导致神经退行性疾病的一个因素，包括阿尔茨海默病（AD）。线粒体是具有多种功能的信号细胞器，从能量产生到细胞代谢、能量稳态和应激反应的调节。这些复杂过程的成功运作严重依赖于线粒体动态的准确性，这包括线粒体在细胞中改变形状和位置的能力，这对于维持适当的功能和质量控制是必要的，尤其是在神经元等极化细胞中。有大量证据表明，线粒体动力学的破坏可能在 AD 的发病机制中起关键作用。本综述强调了 AD 中线粒体动力学改变的各个方面，这些改变可能有助于这种使人衰弱的疾病的病因。我们还讨论了改善线粒体动力学和功能的治疗策略，这可能为提供一种替代治疗方法。
