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巨衍生的CTSS驱动了血液-CSF屏障的年龄依赖性破坏

Yifan Chen¹, Yifei Zhou¹, Yaqing Bai¹

¹State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai 200031, China; University of Chinese Academy of Sciences, Beijing 100049, China.

|February 27, 2025

概括

陈旧的状结质巨细胞分泌着甲素S (CTSS),降低了血液-中枢流体屏障. 抑制CTSS使大脑功能复苏,揭示了老化大脑疾病的目标.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
衰老研究研究衰老研究

背景情况:

胸膜 (CP) 产生脑脊液 (CSF),并通过表皮紧密结节维持血液-脑脊液屏障 (BCB).
这种BCB对大脑平衡至关重要,但其衰老机制尚不清楚.
与年龄相关的神经障碍与BCB功能障碍有关.

研究的目的:

为了研究底层的分子机制胆脉衰老和血液-CSF屏障的下降.
为了确定潜在的治疗目标,以改善老化中的大脑功能.

主要方法:

在老年状交中分析甲素S (CTSS) 表达.
调查CTSS在裂解紧接蛋白质克劳丁1 (CLDN1) 的作用.
评估CTSS抑制或CLDN1上调对老年CP和动物模型中的大脑功能的影响.

主要成果:

在老年人中,由于细胞衰老的增加,CTSS在CP上调节.
CTSS分裂了CLDN1,导致血液-中枢神经液屏障功能受损.
抑制CTSS或恢复CLDN1会使老化的血液-中枢神经液屏障和大脑功能复苏.

结论:

一个涉及CP巨细胞,CTSS和CLDN1的新机制加速了CP和大脑衰老.
在老年人中,CTSS代表了增强大脑平衡的潜在治疗标.
循环蛋白酶在衰老过程中起着至关重要的作用.

关键词:

衰老的衰老衰老的衰老血脑脊髓液屏障血脑脊髓液屏障血脑脊髓液屏障在 cathepsin 中.冠状腺复合体冠状腺复合体认知障碍是一种认知障碍.巨细胞是一个巨细胞.神经炎症是一种神经炎症.紧密的交叉路口紧密的连接

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