时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
Nevertheless, whether EE can prevent schizophrenia-relevant abnormalities induced by ELS, and whether its beneficial effects are confined to specific developmental windows, remain open questions.Adolescence represents a critical neurodevelopmental window characterized by ongoing synaptic pruning, dendritic remodeling, and circuit refinement, especially within the hippocampus [13].；However, whether these alterations causally converge to disrupt CREB-BDNF-TrkB signaling—and whether this pathway can be developmentally targeted for intervention—remains unclear.；In addition, the translational relevance of this pathway, particularly whether its disruption can be detected using peripheral biomarkers, has not been established.In the present study, we investigated whether EE during adolescence can prevent the emergence of schizophrenia-related behavioral and neurobiological abnormalities induced by ELS.
方法
Consistent with this trajectory, we previously demonstrated that MS-induced behavioral abnormalities manifest in adulthood but not during adolescence [7], highlighting adolescence as a critical period for intervention.At the molecular level, the CREB-BDNF-TrkB signaling pathway is a central regulator of synaptic plasticity and cognitive function.；Reduced BDNF expression has been consistently reported in the hippocampus of patients with schizophrenia [16], while phosphorylated CREB (p-CREB) is essential for activity-dependent BDNF transcription and long-term synaptic plasticity.；In addition, the translational relevance of this pathway, particularly whether its disruption can be detected using peripheral biomarkers, has not been established.In the present study, we investigated whether EE during adolescence can prevent the emergence of schizophrenia-related behavioral and neurobiological abnormalities induced by ELS.
核心结论
Converging evidence indicates that ELS induces long-lasting neurobiological alterations, including neuroinflammation, mitochondrial dysfunction, and neuronal apoptosis, particularly within the hippocampus, a key region for cognition and emotional regulation [5, 6].；Consistent with this trajectory, we previously demonstrated that MS-induced behavioral abnormalities manifest in adulthood but not during adolescence [7], highlighting adolescence as a critical period for intervention.At the molecular level, the CREB-BDNF-TrkB signaling pathway is a central regulator of synaptic plasticity and cognitive function.；Consistent with these mechanisms, our previous studies demonstrated increased ROS production and elevated pro-inflammatory cytokines in the hippocampus following MS [19].
局限
However, effective strategies to prevent or reverse these ELS-induced neurodevelopmental abnormalities remain limited.Environmental enrichment (EE) has emerged as a promising non-pharmacological approach to enhance neuroplasticity and behavioral resilience in neurodevelopmental and psychiatric disorders [11, 12].；However, whether these alterations causally converge to disrupt CREB-BDNF-TrkB signaling—and whether this pathway can be developmentally targeted for intervention—remains unclear.；However, SE-MS rats exhibited a reduced spontaneous alternation rate, indicative of impaired working memory, which was significantly improved by EE (Fig. 1F).
对本项目的价值
中高价值：属「线粒体质量控制与氧化应激」方向；线粒体功能与氧化应激栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 52,858 字符，题名指纹 0.76，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：青春期环境丰富化经恢复 CREB-BDNF-TrkB 信号预防早期应激致精神分裂样表型
- 英文标题：Adolescent environmental enrichment prevents early-life stress-induced schizophrenia-like phenotypes via restoration of CREB-BDNF-TrkB signaling.
- 期刊与标识：Translational psychiatry · PMID 42971975 · DOI 10.1038/s41398-026-04388-6 · PMC PMC13728131