线粒体功能障碍是衰老过程中的关键事件:从突触失效到记忆丧失

C. Jara, Angie K. Torres, Margrethe A. Olesen, Cheril Tapia-Rojas
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引用次数: 12

摘要

线粒体是重要的细胞器,在能量产生、氧化平衡和钙稳态中具有关键的调节功能。这在大脑中尤其重要,因为神经元需要大量的功能性线粒体来提供其高能量需求,主要用于突触过程。大脑中,特别是海马体中线粒体活性和质量的下降与正常衰老和大量损害记忆功能的神经退行性疾病有关。尽管突触和认知功能障碍是多因素的,但越来越多的证据表明,线粒体在这些过程中起着关键作用,并表明维持线粒体功能可以防止这些年龄依赖性的改变。在本章中,我们将讨论衰老过程中海马线粒体功能障碍,以及这些缺陷如何促进与年龄相关的突触损伤和认知障碍。我们将总结的证据表明,如何神经退行性变可以通过调节线粒体功能在衰老过程中加速或减弱。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mitochondrial Dysfunction as a Key Event during Aging: From Synaptic Failure to Memory Loss
Mitochondria are important cellular organelles with key regulatory functions in energy production, oxidative balance, and calcium homeostasis. This is especially important in the brain, since neurons require a large number of functional mitochondria to supply their high energy requirement, mainly for synaptic processes. A decrease in the activity and quality of mitochondria in the brain, particularly in the hippocampus, is associated with normal aging and a large number of neurodegenerative diseases compromising memory function. Although synaptic and cognitive dysfunction is multifactorial, growing evidence demonstrates that mitochondria play a key role in these processes and suggests that maintaining mitochondrial function could prevent these age-dependent alterations. In this chapter, we will discuss the hippocampal mitochondrial dysfunction present in aging and how these defects promote age-associated synaptic damage and cognitive impairment. We will summarize evidence that shows how neurodegeneration can be accelerated or attenuated during aging by modulating mitochondrial function.
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