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突触性线粒体糖化有助于线粒体压力和认知功能障碍

Sourav Samanta¹, Firoz Akhter², Renhao Xue²

¹Department of Surgery, Columbia University Vagelos College of Physicians and Surgeons, New York, NY 10032, USA.

Brain : a journal of neurology

|July 13, 2024

概括

先进的糖化终产品 (AGEs) 在老年大脑中损害了突触线粒体. 增强glyoxalase 1 (GLO1) 清除有毒代谢物,改善线粒体和认知功能.

科学领域:

神经科学是一个神经科学.
代谢途径代谢途径
衰老的研究研究.

背景情况:

线粒体和突触功能障碍是大脑衰老和认知衰退的标志.
突触线粒体对于神经元的能量需求至关重要,但它们与与年龄相关的代谢变化的联系尚不清楚.

研究的目的:

调查先进的糖化最终产品 (AGE) 介导的线粒体和突触应激.
评估消除AGE和相关有毒代谢物的策略.
确定神经元氧酶1 (GLO1) 在减轻 AGE 诱导损伤中的作用.

主要方法:

使用了老年小鼠和转基因小鼠过度表达神经元GLO1.
在突触线粒体中分析了AGE和代谢物积累.
评估了线粒体功能,氧化应激和认知表现.
在海马神经元中进行了ex vivo和体外电生理学记录 (LTP,mEPSC).

主要成果:

突触线粒体是AGE和甲基醇 (MG) 的早期和主要目标.
暴露于MG/AGE会损害突触线粒体功能,并增加氧化应激.
增加神经元GLO1活动减少了AGE的积累,并改善了线粒体/认知功能.
神经元GLO1拯救了AGE引起的突触可塑性和传播的缺陷.

结论:

突触线粒体极易受到AGE诱导的损伤,导致与年龄相关的认知衰退.
增加GLO1功能提供了一种治疗策略,以对抗AGE积累.
准AGE和增强GLO1可能会改善线粒体健康和衰老中的认知功能.

关键词:

AGEs的新陈代谢格利奥克萨拉斯 I 酶线粒体和氧化应激的压力.合成线粒体中毒性合成线粒体中毒性突触传输/受伤的发生

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