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C3-C3aR轴通过突触吞,暗微质和PANoptosis驱动罗农诱导的认知损伤

Jianing Liu¹, Liyan Hou², Yu Ma¹

¹School of Public Health, Dalian Medical University, No. 9 W. Lvshun South Road, Dalian, 116044, China.

|February 4, 2026

概括

补充C3 (C3) 和它的受体 (C3aR) 通过促进神经炎症和神经元死亡来驱动帕金森病 (PD) 的认知衰退. 阻止这种C3-C3aR通路为PD提供了潜在的治疗策略.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
病理学病理学病理学

背景情况:

认知障碍是帕金森病 (PD) 中的主要非运动症状,严重影响患者的生活质量.
与PD相关的认知功能障碍背后的精确机制尚未完全理解,因此需要进一步研究诸如神经炎症等促成因素.

研究的目的:

调查补充C3 (C3) 途径在罗诺诱导的帕金森病小鼠模型认知障碍的发病过程中的作用.
阐明C3有助于神经退行,神经炎症和PD认知衰退的分子机制.

主要方法:

利用罗诺诱导的小鼠模型来模仿PD病理和认知缺陷.
研究了C3缺乏和C3a受体 (C3aR) 抑制 (使用SB290157) 对神经炎症,神经元完整性,突触功能和认知表现的影响.
检查了微质激活,暗微质表型,血脑屏障 (BBB) 完整性和与PANoptosis相关的标志物.
进行了体外实验,以探索C3-C3aR轴通过线粒体活性氧物种 (ROS) 和Z-DNA结合蛋白1 (ZBP-1) 在PANoptosis中的作用.

主要成果:

轮暴露上调了微质和神经元中的星细胞C3和C3aR表达,与认知缺陷相关.
C3缺乏或C3aR抑制改善了神经退行,α-synuclein酸化,微质激活和突触修剪,改善了认知功能.
阻断C3-C3aR轴恢复了BBB完整性,减少了神经元亡 (TUNEL阳性细胞),并抑制了PANoptosis.
在体外研究证实,C3-C3aR轴通过线粒体ROS和ZBP-1相互作用促进PANoptosis.

结论:

C3-C3aR轴是一个关键的调解器,将神经炎症,异常突触修剪,暗色微质,BBB干扰和神经元PANoptosis与帕金森病中的认知衰退联系起来.
准C3-C3aR通路为缓解PD患者认知障碍提供了一个有希望的治疗途径.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.在C3aR中,它是C3aR.补充C3 补充C3 补充尸体灭 (Necroptosis) 是一种死亡的过程.神经炎症是一种神经炎症.帕金森病的疾病.

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