Mitochondrial respiratory capacity is not altered in aging rat brains with or without memory impairment.

microPublication biology Pub Date : 2024-10-21 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001359
Pamela J Yao, Jeffrey M Long, Peter R Rapp, Dimitrios Kapogiannis
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Abstract

Mitochondria are essential for supporting the high metabolic demands that are required for brain function. Impairments in mitochondria have been linked to age-related decline in brain functions. Here, we investigate whether the mitochondrial respiratory capacity of brain cells is changed in cognitive aging. We used a rat model of normal cognitive aging and analyzed mitochondrial oxidative phosphorylation in frozen brain samples. Mitochondrial oxygen consumption rate analysis of the frontal cortex did not show any differences between young rats and aged rats with either intact memory or impaired spatial memory. Mitochondrial ATP synthase activity and quantity also did not differ between young and aged rats. These results suggest that the total level of mitochondrial respiratory capacity is preserved in the frontal cortex of aged rats and may not explain aging-associated cognitive impairment.

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无论是否存在记忆损伤,衰老大鼠大脑的线粒体呼吸能力都不会发生改变。
线粒体对于支持大脑功能所需的高代谢需求至关重要。线粒体的损伤与年龄相关的大脑功能衰退有关。在此,我们研究了认知衰老是否会改变脑细胞线粒体的呼吸能力。我们利用正常认知衰老的大鼠模型,分析了冷冻脑样本中线粒体的氧化磷酸化。对额叶皮层线粒体耗氧率的分析表明,年轻大鼠与空间记忆力完好或受损的老年大鼠之间没有任何差异。线粒体 ATP 合成酶的活性和数量在年轻大鼠和老年大鼠之间也没有差异。这些结果表明,在老年大鼠的额叶皮层中,线粒体呼吸能力的总水平得以保留,这可能无法解释与衰老相关的认知障碍。
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