癫痫发生
调解人
神经科学
封锁
化学
发作性
癫痫
药理学
神经传递
运动前神经元活动
中和
突触后电位
突触可塑性
丙戊酸
抗惊厥药
神经递质
突触
临床神经学
作者
Yoonyi Jeong,Hyun‐Kyoung Lim,Hayeon Kim,Juheon Lee,S H. Lee,Minah Suh
出处
期刊:Epilepsia
[Wiley]
日期:2025-10-21
卷期号:67 (2): 908-922
被引量:3
摘要
Our findings demonstrate that C1q acts as an upstream mediator of complement-driven neuronal loss during epileptogenesis. C1q blockade interrupted the pathogenic cascade involving microglial engulfment and astrocytic C3 upregulation, thereby preserving synaptic and neuronal integrity and reducing interictal spike activity. Our study highlights the therapeutic potential of C1q inhibition, which can provide multifaceted benefits by mitigating neuroinflammation, improving synaptic integrity, and reducing epileptiform activity during epileptogenesis.
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