Mitochondrial Fragmentation as a Key Driver of Neurodegenerative Disease.

Alina Chaplygina, Daria Zhdanova
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Abstract

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.

线粒体断裂是神经退行性疾病的关键驱动因素。
线粒体的形态和功能通过融合和裂变的动态过程错综复杂地联系在一起,这些过程中的破坏是神经退行性疾病的关键驱动因素,如阿尔茨海默氏症。线粒体无法在其动态形式之间转换是病理状态发展的关键因素。在本文中,我们关注不同类型线粒体表型在神经组织中的重要性,讨论阿尔茨海默病中的线粒体如何“卡住”在某些模式中,以及这种模式如何维持自身。了解线粒体形态(包括微小的、网络化的和高灌注的)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,我们可能能够在疾病过程的早期进行干预,为预防或治疗神经变性提供新的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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