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急性阻断过度的线粒体分裂可以防止创伤性脑损伤后的慢性神经退行

Preethy S Sridharan¹, Yeojung Koh², Emiko Miller¹

¹Department of Psychiatry, Case Western Reserve University School of Medicine, Cleveland, OH, USA; Brain Health Medicines Center, Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; Geriatric Psychiatry, GRECC, Louis Stokes VA Medical Center, Cleveland, OH, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA; Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

Cell reports. Medicine

|September 6, 2024

概括

急性创伤性脑损伤 (TBI) 可以导致慢性神经退行. 在小鼠TBI后不久抑制线粒体分裂蛋白Fis1可以防止长期的大脑损伤和认知能力下降.

科学领域:

神经科学是一个神经科学.
线粒体生物学线粒体生物学
创伤性脑损伤研究研究

背景情况:

创伤性脑损伤 (TBI) 进展为慢性神经退行症缺乏有效的保护性治疗方法.
线粒体动力学,特别是裂变,与TBI后的神经退行过程有关.

研究的目的:

研究线粒体分裂蛋白1 (Fis1) 在TBI引起的慢性神经退行症中的作用.
评估TBI后抑制Fis1-dynamin相关蛋白1 (Drp1) 相互作用的治疗潜力.

主要方法:

利用TBI的小鼠模型研究线粒体裂变和Fis1水平.
在TBI后两周内使用药理抑制剂,针对Fis1-Drp1相互作用.
评估了长期结果,包括线粒体功能,氧化损伤,神经炎症,血脑屏障完整性,神经退行和认知表现.

主要成果:

在TBI后在小鼠中观察到急剧升高的线粒体裂变和Fis1水平,在人类TBI大脑中也发现了升高的Fis1.
早期药理上抑制Fis1-Drp1结合可以预防慢性线粒体功能障碍,氧化应激,神经炎症,BBB损伤,神经退行和认知缺陷.
延迟治疗 (TBI后8个月) 显示没有保护作用,突出了干预的关键时间窗口.

结论:

由Fis1介导的急剧升高的线粒体裂变是TBI后慢性神经退行的一个关键驱动因素.
在TBI后不久,对Fis1-Drp1相互作用的时间敏感抑制是预防人类患者长期神经损伤和认知障碍的有希望的治疗策略.

关键词:

DRP1 是一个DRP1 财政财政财政财政财政财政血脑屏障是什么意思线粒体中的线粒体.线粒体分裂的线粒体裂变线粒体融合是指线粒体的融合.神经退行症的神经退行症神经保护神经保护氧化应激是一种氧化应激.创伤性脑损伤是一种创伤性脑损伤.

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