Li Huashan, Yu Wanqiu, Zheng Xue, Zhu Zhaoqiong
Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563003, China; Department of Anesthesiology, Zunyi Maternal And Child Health Care Hospital, Zunyi 563000, China.
Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, Zunyi 563003, China.
Brain Res Bull. 2025 Jan;220:111162. doi: 10.1016/j.brainresbull.2024.111162. Epub 2024 Dec 5.
Neurocognitive Disorders (NCDs) primarily affect cognitive functions, including learning, memory, perception, and problem-solving. They predominantly arise as pathological sequelae of central nervous system (CNS) disorders. Emerging evidence suggests that microglial inflammatory activation within the hippocampus underlies the pathogenesis of cognitive impairment. Triggering receptor expressed on myeloid cells 1 (TREM1), a pattern-recognition receptor on microglia, becomes upregulated in response to injury and synergistically amplifies inflammatory responses mediated by other pattern-recognition receptors, leading to uncontrolled inflammation. While TREM1 is lowly expressed in the resting state, its upregulation upon exposure to injurious inflammatory stimuli promotes microglial activation and contributes to the development of NCDs. Consequently, TREM1 may serve as a critical receptor in microglia-mediated inflammation. This article reviews the current understanding of TREM1 and its role in NCDs pathogenesis.
神经认知障碍(NCDs)主要影响认知功能,包括学习、记忆、感知和问题解决能力。它们主要作为中枢神经系统(CNS)疾病的病理后遗症出现。新出现的证据表明,海马体内小胶质细胞的炎症激活是认知障碍发病机制的基础。髓系细胞表达的触发受体1(TREM1)是小胶质细胞上的一种模式识别受体,在受到损伤时会上调,并协同放大由其他模式识别受体介导的炎症反应,导致炎症失控。虽然TREM1在静息状态下表达较低,但在暴露于有害炎症刺激时其上调会促进小胶质细胞激活,并促成NCDs的发展。因此,TREM1可能是小胶质细胞介导的炎症中的关键受体。本文综述了目前对TREM1及其在NCDs发病机制中作用的理解。