大脑[NAD+]/[NADH]和[NADPH]/[NADP+]的变化随着衰老和抗衰老饮食限制
Leah E Jamerson1, Tara D Bradshaw2, Patrick C Bradshaw1
1Department of Biomedical Sciences, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, United States.
Frontiers in aging neuroscience
|February 20, 2026
概括
通过NAD+和NADPH比率测量的大脑氧化还原状态,随着衰老和禁食而变化. 间歇性禁食诱导有益的减速转移,可能延迟衰老和促进神经保护.
科学领域:
- 神经科学是一个神经科学.
- 代谢过程中的代谢.
- 衰老研究研究 衰老研究
背景情况:
- 大脑的氧化还原平衡,以[NADPH]/[NADP+]和[NAD+]/[NADH]比率来表示,与衰老有关.
- 饮食限制 (DR) 和间歇性禁食 (IF) 影响氧化还原状态,可能会调解它们的抗衰老作用.
研究的目的:
- 为了研究老化和IF如何影响大脑氧化还原状态,使用特定的代谢物对作为指标.
- 探索氧化还原变化,衰老和IF诱导的神经保护之间的关系.
主要方法:
- 使用的代谢物对比 (pyruvate/lactate,acetoacetate/beta-hydroxybutyrate,malate/pyruvate,isocitrate/alpha-ketoglutarate) 作为细胞质和线粒体的氧化还原状态的指标.
- 从老化和DR模型中分析了大脑蛋白质组和RNA-Seq数据.
- 在C57BL/6J小鼠,C57BL/6N小鼠和人类中比较了氧化还原变化.
主要成果:
- 与C57BL/6N小鼠和人类相比,C57BL/6J小鼠大脑中的衰老诱导的相反的细胞质氧化还原变化.
- IF导致大脑细胞质和线粒体氧化还原状态的普遍还原性转移.
- IF在细胞质[NAD+]/[NADH]中的还原性转移与基补充剂的氧化转移形成对比.
结论:
- 间歇性禁食促进有益的循环还原氧化转移在大脑中,特别是在线粒体.
- 这些氧化还原转移可能驱动与IF相关的神经保护和抗衰老效应.
- 了解这些代谢途径是制定健康衰老策略的关键.
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