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童年期创伤通过免疫炎症途径影响精神分裂症快感缺失的研究进展

  • 刘文霞 ,
  • 张晨
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  • 1.上海市长宁区精神卫生中心精神科,上海 200335
    2.上海交通大学医学院附属精神卫生中心精神科,上海 200030
张 晨,主任医师,博士;电子信箱:zhangchen645@gmail.com

收稿日期: 2025-06-18

  录用日期: 2025-10-21

  网络出版日期: 2026-02-28

基金资助

国家自然科学基金(82271538);上海市长宁区卫生健康委员会科研基金(2023QN11)

Research advances in the impact of childhood trauma on anhedonia in schizophrenia via immune-inflammatory pathways

  • Liu Wenxia ,
  • Zhang Chen
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  • 1.Department of Psychiatry, Changning District Mental Health Center, Shanghai 200335, China
    2.Department of Psychiatry, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China
Zhang Chen, E-mail: zhangchen645@gmail.com.

Received date: 2025-06-18

  Accepted date: 2025-10-21

  Online published: 2026-02-28

Supported by

National Natural Science Foundation of China(82271538);Science and Research Fund of Changning District Health Commission of Shanghai(2023QN11)

摘要

童年期创伤是精神分裂症发病的重要环境风险因素,通过复杂的生物学编程机制增加个体神经发育异常易感性。快感缺失作为精神分裂症的核心阴性症状之一,表现为对愉悦刺激反应能力的持续减退,严重影响患者的社会功能及长期预后。研究发现,免疫炎症通路的异常激活可能是连接童年期创伤暴露与精神分裂症快感缺失病理过程的关键桥梁。童年期创伤通过持续激活应激与代谢相关生理通路,可导致全身性低度慢性炎症状态,进而引起促炎因子升高、抗炎功能受抑制及神经免疫细胞异常活化等一系列免疫紊乱。这些变化可能进一步通过影响神经功能与环路,介导快感缺失的发生与发展。该文总结现有研究进展,系统阐述童年期创伤对免疫系统的影响及精神分裂症快感缺失的潜在机制,重点分析两者的关联性以及免疫炎症因子在其中所起的介导作用。

本文引用格式

刘文霞 , 张晨 . 童年期创伤通过免疫炎症途径影响精神分裂症快感缺失的研究进展[J]. 上海交通大学学报(医学版), 2026 , 46(2) : 235 -240 . DOI: 10.3969/j.issn.1674-8115.2026.02.013

Abstract

Childhood trauma serves as a significant environmental risk factor for the onset of schizophrenia, and through complex biological programming mechanisms, it increases the susceptibility of individuals to neurodevelopmental abnormalities. Anhedonia, as one of the core negative symptoms of schizophrenia, is characterized by a persistent decline in the ability to respond to pleasurable stimuli, severely affecting the social functions and long-term prognosis of patients. Recent studies have revealed that the abnormal activation of immune-inflammatory pathways may serve as a crucial intermediary link connecting childhood trauma exposure with the pathophysiological process of anhedonia in schizophrenia. Childhood trauma can lead to a systemic low-grade chronic inflammatory state by continuously activating stress- and metabolism-related physiological pathways, which in turn causes a series of immune disorders, such as elevated pro-inflammatory factors, suppressed anti-inflammatory functions, and abnormal activation of neuroimmune cells. These changes may further mediate the occurrence and development of anhedonia by affecting neural functions and circuits. This review summarizes and analyzes current research progress, systematically elaborates the impact of childhood trauma on the immune system and the potential mechanisms of anhedonia in schizophrenia, and focuses on analyzing the correlation between the two and the mediating role of immune-inflammatory factors.

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