Zhang Junhui, Zhang Yanqing, Chen Yuanyuan, Zhu Jianjun
Department of Psychology, Guangzhou University, Guangzhou, China.
Department of Psychology, Guangzhou University, Guangzhou, China.
J Affect Disord. 2025 Oct 15;387:119519. doi: 10.1016/j.jad.2025.119519. Epub 2025 May 27.
Prenatal stress is known to disrupt neurodevelopment in offspring, heightening their risk of mental health disorders. However, its impact on the morphometric similarity network (MSN)-a framework that integrates multiple anatomical features to quantify structural similarity across brain regions in the developing offspring-remains poorly understood.
Using data from the Queensland Twin Adolescent Brain (QTAB) longitudinal study focusing on adolescent twins, we investigated the impact of prenatal stress on cortical MSN in 414 early adolescents (aged 9-14 years). Furthermore, we analyzed the relationship between MSN strength alterations associated with prenatal stress and anatomically organized gene expressions. Disease-related analysis and functional enrichment analysis were conducted.
Adolescents exposed to prenatal stress exhibited smaller age-related changes in MSN strength between ages 9 and 14, particularly in regions associated with emotional regulation, cognitive control, and decision-making, despite showing greater similarity at age 9 compared to their unexposed peers. We identified cortical patterns characterized by weighted gene expression, strongly associated with group differences in MSN strength. Gene expressions linked to prenatal stress-related MSN strength changes were correlated with differential gene expression (DGE) implicated in conditions such as autism spectrum disorder (ASD) and inflammatory bowel disease (IBD).
These results enhance insights into the interplay between gene expression and structural brain changes driven by prenatal stress, highlighting a potential mechanistic link between prenatal stress and neurodevelopmental vulnerability, shedding light on the biological pathways underpinning neurodevelopmental risk factors.
已知产前应激会扰乱后代的神经发育，增加其患精神健康障碍的风险。然而，其对形态测量相似性网络（MSN）的影响——这是一个整合多种解剖特征以量化发育中后代大脑区域结构相似性的框架——仍知之甚少。
利用昆士兰双胞胎青少年大脑（QTAB）纵向研究的数据，该研究聚焦于青少年双胞胎，我们调查了产前应激对414名早期青少年（9至14岁）皮质MSN的影响。此外，我们分析了与产前应激相关的MSN强度改变与解剖学上有组织的基因表达之间的关系。进行了疾病相关分析和功能富集分析。
暴露于产前应激的青少年在9至14岁之间，MSN强度的年龄相关变化较小，特别是在与情绪调节、认知控制和决策相关的区域，尽管与未暴露的同龄人相比，他们在9岁时表现出更大的相似性。我们确定了以加权基因表达为特征的皮质模式，与MSN强度的组间差异密切相关。与产前应激相关的MSN强度变化相关的基因表达与自闭症谱系障碍（ASD）和炎症性肠病（IBD）等疾病中涉及的差异基因表达（DGE）相关。
这些结果增强了对产前应激驱动的基因表达与大脑结构变化之间相互作用的理解，突出了产前应激与神经发育易感性之间潜在的机制联系，揭示了神经发育风险因素背后的生物学途径。
