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Aging synaptic mitochondria exhibit dynamic proteomic changes while maintaining bioenergetic function

机译:老化的突触线粒体表现出动态的蛋白质组学变化同时保持生物能功能

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摘要

Aging correlates with a progressive impairment of mitochondrial homeostasis and is an influential factor for several forms of neurodegeneration. However, the mechanisms underlying age-related alterations in synaptosomal mitochondria, a neuronal mitochondria population highly susceptible to insults and critical for brain function, remain incompletely understood. Therefore this study investigates the synaptic mitochondrial proteomic and bioenergetic alterations that occur with age. The utilization of a state of the art quantitative proteomics approach allowed for the comparison of protein expression levels in synaptic mitochondria isolated from 5 (mature), 12 (old), and 24 (aged) month old mice. During the process of aging we find that dynamic proteomic alterations occur in synaptic mitochondria. Despite direct (mitochondrial DNA deletions) and indirect (increased antioxidant protein levels) signs of mitochondrial damage in the aged mice, there was an overall maintenance of mitochondrial function. Therefore the synaptic mitochondrial proteomic changes that occur with aging correlate with preservation of synaptic mitochondrial function.
机译:衰老与线粒体稳态的进行性损伤有关,并且是几种形式的神经退行性变的影响因素。然而,尚未完全理解突触体线粒体中与年龄有关的改变的机制,突触体线粒体是一种高度易受伤害并且对脑功能至关重要的神经元线粒体。因此,本研究调查了随着年龄增长而发生的突触线粒体蛋白质组学和生物能改变。利用最先进的定量蛋白质组学方法可以比较从5(成熟),12(大)和24(大)月龄小鼠分离的突触线粒体中的蛋白质表达水平。在衰老过程中,我们发现动态蛋白质组学改变发生在突触线粒体中。尽管在衰老小鼠中线粒体受损的直接迹象(线粒体DNA缺失)和间接迹象(抗氧化蛋白水平升高),但线粒体功能总体上得以维持。因此,随着衰老而发生的突触线粒体蛋白质组学变化与突触线粒体功能的保存相关。

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