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对于恢复神经发育突触和认知缺陷而言,细胞骨控制是必不可少的

Sofie Kessels¹, Chloë Trippaers^1,2, Melanie Mertens¹

¹Biomedical Research Institute, BIOMED, Hasselt University, UHasselt, 3590 Diepenbeek, Belgium.

Science advances

|August 29, 2025

概括

对于大脑的健康至关重要. 微质中的DISC1受损会导致突触和记忆缺陷,但恢复微质功能可以扭转这些神经发育障碍的认知障碍.

科学领域:

神经科学
细胞生物学
遗传学

背景情况:

突触功能障碍是神经发育障碍 (NDD) 的关键特征.
微细胞分裂依赖于细胞骨动力学,类似于神经元功能.
支架蛋白DISC1 (精神分裂症中乱的1) 整合了动蛋白结合蛋白.

研究的目的:

调查微性动蛋白细胞骨调节在NDD中的作用.
确定微质中受损DISC1对突触功能和认知的影响.
探索针对微细胞骨动态的治疗潜力.

主要方法:

使用基因工程DISC1缺陷的小鼠来模拟微质功能障碍.
分析了微质细胞中的活性组织和蛋白质吸收.
评估海马刺激传输和空间记忆的表现.
使用骨髓移植重新引入野生类型的微质细胞.

主要成果:

微质中的DISC1受损改变了动蛋白平衡,使其更喜欢细型结构而不是细型结构.
微质失调导致过度的突触蛋白质吸收.
缺少DISC1的小鼠表现出海马突触传输和空间记忆缺陷的减少.
在成年DISC1缺陷小鼠中,野生型微细胞的骨髓移植恢复了突触功能和认知能力.

结论:

在保持突触完整性和认知功能方面,微细胞骨重塑是必不可少的.
由于DISC1受损,导致与NDD相关的认知缺陷.
调节微细胞骨动力学为NDD提供了潜在的治疗策略,即使在成年时也是如此.

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