急性一氧化碳中毒后迟发性脑病(DEACMP)一直未得到医学研究界的重视。我国有4.8亿农村人口仍采用炭火取暖，急性一氧化碳(CO)中毒成为冬季医院急诊的主要病种，其中DEACMP者占1/3。本课题组在急性CO中毒群体中发现，钙黏蛋白基因可能是DEACMP的易感基因，该病具有遗传易感性。神经损伤是该病主要病理表现之一，研究提示钙黏蛋白信号通路与脱髓鞘等神经损伤的修复有关。本研究首先通过独立样本再次验证DEACMP阳性关联基因，然后建立DEACMP大鼠模型，通过神经病理、认知行为和脑电生理对模型进行评价；通过生化检测、RNA干扰和基因过表达、工具药调控等对钙黏蛋白信号通路进行分析，探讨该信号通路能否挽救模型病理改变以及参与DEACMP神经损伤后修复的作用机理。本项目预期将进一步明确DEACMP的易感基因，并初步解释钙黏蛋白信号通路异常与神经损伤的关系，为明确DEACMP发病机理提供实验证据。

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) has not been recognized by the medical research community. There are 480 million rural population is still using charcoal for heating in our country,Acute carbon monoxide(C0) poisoning has become the main disease in winter hospital emergency,including a third of DEACMP. In this study group, we found that the Cadherin gene may be a susceptibility gene of DEACMP, which is a susceptibility gene.Nerve injury is one of the main pathological features of the disease,The study suggests that the signal pathway of Cadherin is related to the repair of nerve injury.In this study, the positive association of DEACMP was tested by independent samples,and then establish the DEACMP rat model,evaluated the model by means of neural pathology, cognitive behavior and EEG,then, analyze the calcium mucin signal pathway by biochemical test, RNA interference and gene over expression, drug control and so on,To investigate whether the signaling pathway can rescue the pathological changes of the model and the mechanisms involved in the repair of DEACMP nerve injury.The project is expected to further clarify the susceptible genes of DEACMP and preliminary explanation the relationship between cadherin signaling pathway and nerve injury, and to provide experimental evidence for the pathogenesis of DEACMP.