Abstract: Cognitive impairment is often manifested as a series of brain function deficits such as learning，memory， intellectual，emotional，and executive deficits. It often occurs in neurological disorders，aging，and the postoperative period. Currently，the pathogenesis of the disease is unclear，and the blood-brain barrier，oxidative stress，autophagy， inflammation，mitochondria，and neurotransmitters have all been implicated in cognitive dysfunction. Recent studies have found that copper homeostasis associated with copper metabolism and copper death has a regulatory role in cognitive function， which may be a key mechanism in the development of cognitive impairment. In this paper，we systematically introduce the role of copper homeostasis regulatory mechanisms in cognitive impairment from the perspectives of mitochondria，glial cells，oxidative reactions，inflammatory factors，neurotransmitters，etc.（when copper homeostasis is imbalanced，copper ion levels are disturbed，electrolyte metabolism is abnormal，and a series of reactions，such as oxidative stress，inflammatory aggregation， mitochondrial disorders，and glial cell damage，occur，and even induce neuronal copper death）and summarise the role of copper homeostasis in cognitive impairment. The role of copper homeostasis in cognitive disorders is summarised， to provide new insights into the pathogenesis of cognitive disorders，as well as bringing new solutions to the treatment of the disease.

Key words: Cognitive impairment, Copper steady state, Copper metabolism, Copper death, Review

摘要： 认知障碍常表现为学习、记忆、智力、情感、执行力障碍等一系列脑功能缺损表现，常发生在神经功能疾病、衰老、术后等中。目前，认知障碍的发病机制尚不明确，血 - 脑脊液屏障、氧化应激、自噬、炎症、线粒体以及神经递质均与认知障碍有关。最近研究发现，铜代谢和铜死亡相关的铜稳态对认知功能有调控作用，这可能是认知障碍发生、发展中的关键机制。本文从线粒体、胶质细胞、氧化应激、炎症因素、神经递质等角度系统地介绍了铜稳态调控机制在认知障碍中的作用（铜稳态失衡时，铜离子水平紊乱，电解质代谢异常，发生氧化应激、炎症聚集、线粒体紊乱、胶质细胞损伤等一系列反应，甚至诱导神经元发生铜死亡），并对铜稳态在认知障碍中所起的作用进行了总结，以期为认知障碍发病机制提供新的见解，同时也期待给该病的治疗带来新的方案。

关键词: 认知障碍, 铜稳态, 铜代谢, 铜死亡, 综述