Chaplygina Alina, Zhdanova Daria
Institute of Cell Biophysics, Russian Academy of Sciences - A Separate Division of Federal Research Center Pushchino Research Center for Biological Studies, Russian Academy of Sciences (ICB RAS), Moscow, 142290, Russia.
Curr Alzheimer Res. 2024;21(9):607-614. doi: 10.2174/0115672050366194250107050650.
Mitochondrial form and function are intricately linked through dynamic processes of fusion and fission, and disruptions in these processes are key drivers of neurodegenerative diseases, like Alzheimer's. The inability of mitochondria to transition between their dynamic forms is a critical factor in the development of pathological states. In this paper, we focus on the importance of different types of mitochondrial phenotypes in nervous tissue, discussing how mitochondria in Alzheimer's disease are "stuck" in certain patterns and how this pattern maintains itself. Understanding the specific roles and transitions between mitochondrial forms, including tiny, networked, and hyperfused, is crucial in developing new therapies aimed at restoring mitochondrial homeostasis. By targeting these dynamics, we may be able to intervene early in the disease process, offering novel avenues for preventing or treating neurodegeneration.
线粒体的形态与功能通过融合与裂变的动态过程紧密相连，而这些过程的紊乱是神经退行性疾病（如阿尔茨海默病）的关键驱动因素。线粒体无法在其动态形态之间转变是病理状态发展的一个关键因素。在本文中，我们聚焦于神经组织中不同类型线粒体表型的重要性，探讨阿尔茨海默病中的线粒体是如何“陷入”某些模式以及这种模式是如何自我维持的。了解线粒体形态（包括微小、网络化和过度融合）之间的具体作用和转变，对于开发旨在恢复线粒体稳态的新疗法至关重要。通过针对这些动态变化，我们或许能够在疾病进程的早期进行干预，为预防或治疗神经退行性变提供新途径。
