细胞黏附分子Nectin-1在癫痫认知障碍的可能机制

Potential roles of nectin-1 in cognitive impairment in epilepsy

摘要:

癫痫是最常见的神经系统疾病之一，认知障碍是癫痫常见的并发症，严重影响患者的生活质量，而其发病机制较复杂且目前未研究清楚。突触可塑性是癫痫及认知障碍发生的重要机制，近年来越来越多的研究证实，细胞黏附分子Nectin-1在突触可塑性中发挥重要的作用，且在癫痫模型大鼠的海马组织异常表达，并通过影响突触可塑性引起癫痫的发生、认知功能障碍。现就细胞黏附分子Nectin-1在癫痫认知障碍的可能机制进行综述，以期寻求潜在的干预措施。

Abstract:

Epilepsy is one of the most common nervous system diseases. Cognitive impairment is a common complication of epilepsy and seriously affects the quality of life of patients. However, the pathogenesis of cognitive impairment in epilepsy is complex and has not been clearly studied yet. Synaptic plasticity is an important mechanism underlying the occurrence of epilepsy and cognitive impairment. In recent years, more and more studies have confirmed that cell adhesion molecule nectin-1 plays an essential role in synaptic plasticity. Nectin-1 is abnormally expressed in the hippocampus of rat models of epilepsy, and causes epilepsy and cognitive impairment by affecting the synaptic plasticity. This review summarizes the possible roles of cell adhesion molecule nectin-1 in cognitive impairment in epilepsy with a view to exploring potential intervention measures.