术后认知功能障碍（postoperative cognitive dysfunction，POCD）是手术后常见并发症，不仅影响术后 患者的康复，延长住院时间，还可能增加术后死亡的风险。N-甲基-D-天冬氨酸（N-methyl-D-aspartate， NMDA）受体在学习、记忆和突触可塑性中发挥着关键作用，并在POCD的发生发展中扮演重要角色。包括 手术应激，炎症和疼痛在内的围手术期因素均会导致NMDA受体过度激活。本综述首次整合了临床前和 临床研究，讨论因围手术期损伤，疼痛和炎症多因素诱导的NMDA受体过度激活促进POCD发生及进展的 作用机制，旨在挖掘POCD的有效治疗靶点，为改善患者术后认知功能的精准临床治疗策略提供参考。

Postoperative cognitive dysfunction (POCD), a prevalent post-surgical complication, not only hampers patient recovery and prolongs hospital stays but also potentially increases the risk of postoperative mortality. N-methyl-D-aspartate (NMDA) receptors, pivotal for learning, memory, and synaptic plasticity, play crucial roles in the development and progression of POCD. Perioperative factors, such as surgical stress, inflammation, and pain, can result in excessive activation of NMDA receptors. This review synthesizes findings from both preclinical and clinical studies for the first time, discussing the mechanisms by which overactivation of NMDA receptors, triggered by multifactorial perioperative insults such as injury, pain, and inflammation, contributes to the development and advancement of POCD. The aim of this review is to identify effective therapeutic targets for POCD and provide guidance for precision clinical treatment strategies that improve postoperative cognitive function in patients.