Nishitani Shota, Fujisawa Takashi X, Takiguchi Shinichiro, Yao Akiko, Murata Kazuhiro, Hiraoka Daiki, Mizuno Yoshifumi, Ochiai Keiko, Kawata Natasha Y S, Makita Kai, Saito Daisuke N, Mizushima Sakae, Suzuki Shizuka, Kurata Sawa, Ishiuchi Naoki, Taniyama Daiki, Nakao Naoki, Namera Akira, Okazawa Hidehiko, Nagao Masataka, Tomoda Akemi
Research Center for Child Mental Development, University of Fukui, Fukui, Japan.
Division of Developmental Higher Brain Functions, United Graduate School of Child Development, Osaka University, Kanazawa University, Hamamatsu University School of Medicine, Chiba University, and University of Fukui, Osaka, Japan.
Mol Psychiatry. 2025 Sep 16. doi: 10.1038/s41380-025-03236-1.
Child maltreatment (CM) is associated with adverse physical, psychological, and neurodevelopmental outcomes later in life. Epigenetic modifications, particularly DNA methylation, have been proposed as potential mechanisms underlying these long-term effects. To identify robust CM-associated methylation signatures, we conducted epigenome-wide analyses across three independent cohorts: judicial autopsy cases (CM:11, Controls:7), toddlers shortly after social intervention (CM:36, Controls:49), and adolescents who underwent brain MRI (CM:61, Controls:62). Each cohort was analyzed separately, followed by a meta-analysis to identify common methylation sites associated with CM exposure. The meta-analysis identified four significant CpG sites located within the ATE1, SERPINB9P1, CHST11, and FOXP1 genes. Among these, methylation of FOXP1 was consistently associated with structural brain alterations, including increased gray matter volume (GMV) in the orbitofrontal cortex (OFrC) and middle/posterior cingulate gyrus (MPCG), and decreased GMV in the occipital fusiform gyrus (OFuG). These brain regions are implicated in emotional regulation, memory retrieval, and social cognition, suggesting a potential neurobiological mechanism linking CM to later psychopathology. Furthermore, methylation risk scores (MRS) derived from these four CpGs successfully discriminated individuals who experienced early-life adversity in an independent validation dataset, achieving an area under the receiver operating characteristic curve (AUC) of 0.672, highlighting their potential utility as biomarkers. Gene ontology and pathway analyses revealed enrichment of cholinergic and glutamatergic synaptic transmission pathways, supporting their involvement in traumatic memory formation. Our findings provide novel insights into the epigenetic mechanisms underlying CM and identify potential biomarkers for early detection, prevention, and therapeutic intervention, ultimately contributing to breaking the intergenerational cycle of maltreatment.
儿童虐待(CM)与日后生活中不良的身体、心理和神经发育结果相关。表观遗传修饰,尤其是DNA甲基化,被认为是这些长期影响的潜在机制。为了识别与CM相关的稳健甲基化特征,我们在三个独立队列中进行了全表观基因组分析:司法尸检案例(CM:11例,对照:7例)、社会干预后不久的幼儿(CM:36例,对照:49例)以及接受脑部MRI检查的青少年(CM:61例,对照:62例)。每个队列分别进行分析,随后进行荟萃分析以识别与CM暴露相关的常见甲基化位点。荟萃分析确定了位于ATE1、SERPINB9P1、CHST11和FOXP1基因内的四个显著CpG位点。其中,FOXP1的甲基化与大脑结构改变始终相关,包括眶额皮质(OFrC)和中/后扣带回(MPCG)灰质体积(GMV)增加,以及枕颞梭状回(OFuG)GMV减少。这些脑区与情绪调节、记忆检索和社会认知有关,提示了一种将CM与后期精神病理学联系起来的潜在神经生物学机制。此外,从这四个CpG得出的甲基化风险评分(MRS)在一个独立验证数据集中成功区分了经历过早期生活逆境的个体,受试者工作特征曲线下面积(AUC)为0.672,突出了它们作为生物标志物的潜在效用。基因本体和通路分析显示胆碱能和谷氨酸能突触传递通路富集,支持它们参与创伤性记忆形成。我们的发现为CM潜在的表观遗传机制提供了新见解,并识别出用于早期检测、预防和治疗干预的潜在生物标志物,最终有助于打破虐待的代际循环。