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颞叶癫痫(Temporal lobe epilepsy,TLE)是最常见的癫痫类型,大部分为药物难治性癫痫,最主要的病理特征是海马苔藓纤维出芽和突触重塑,是目前研究的热点。国内外许多学者运用比较蛋白质组学技术,通过比较TLE患者或动物模型组与对照组的差异蛋白质,发现脑衰反应调节蛋白2(CRMP-2)的表达下调最显著,表明CRMP-2与TLE密切相关。CRMP-2属于细胞质磷蛋白,高表达于中枢神经系统,尤其是神经元和少突胶质细胞。通过对CRMP-2表达信号通路作用机制的相关性研究,CRMP-2在经典通路中通过影响神经元微管的合成从而调节轴突和树突的生长,推测CRMP-2在TLE海马神经元损伤的作用是通过PTEK/P13K/Akt/GSK-3β/CRMP-2信号通路进行的,可揭示TLE的发病机制及为进一步的临床治疗提供新的作用靶点。
Temporal lobe epilepsy (TLE) is the most common type of epilepsy, most of them are refractory epilepsy. The main pathological features are the sprouting and synaptic remodeling of mossy fiber in the hippocampus. Many scholars at home and abroad use comparative proteomics technology to find out that the expression of CRMP-2 is down-regulated most by comparing the difference proteins of TLE patients or animal models with that of the control group, indicating that CRMP-2 and TLE closely related. CRMP-2 is a cytoplasmic phosphoprotein that is highly expressed in the central nervous system, especially neurons and oligodendrocytes. CRMP-2 regulates the growth of axons and dendrites by affecting the synthesis of neuronal microtubules in the classical pathway, suggesting that CRMP-2 may play an important role in the neuronal damage of TLE hippocampus Through the PTEK / P13K / Akt / GSK-3β / CRMP-2 signaling pathway, can reveal the pathogenesis of TLE and provide a new target for further clinical treatment.