犬尿氨酸途径
萧条(经济学)
联想(心理学)
全基因组关联研究
基因组
计算生物学
遗传学
生物
医学
犬尿氨酸
心理学
基因
基因型
色氨酸
心理治疗师
宏观经济学
单核苷酸多态性
经济
氨基酸
作者
Yaoyao Sun,Yundan Liao,Yuyanan Zhang,Zhe Lü,Yuzhuo Ma,Zhewei Kang,Xiaoyang Feng,Guorui Zhao,Junyuan Sun,Yunqing Zhu,M. Yuan,Yang Yang,Liangkun Guo,Xiao Zhang,Dai Zhang,Runsen Chen,Wenjian Bi,Weihua Yue
标识
DOI:10.1038/s41467-025-57066-4
摘要
Childhood maltreatment stands out as a pivotal risk factor for depression, with gene-by-environment interaction serving as a crucial mechanism. Here we perform genome-wide interaction analyzes of childhood maltreatment in the UK Biobank, integrating methylation evidence through colocalization analysis and identifying associated brain structure abnormalities from childhood to adulthood. A genome-wide significant genomic region interacting with childhood maltreatment is identified at 8p11.21 (IDO2 rs7846217, P = 2.02e-08), implicating the tryptophan-kynurenine pathway. Colocalization analysis reveals that IDO2 rs11777027, rs2340953 and rs28631334 are associated with depression in individuals exposed to childhood maltreatment and colocalize with methylation signals in both blood and brain for IDO2. These interactions affect cortical thickness of the left supramarginal gyrus in children (P = 9.72e-04) and adults (P = 1.34e-04), as well as cortical volume in the right angular gyrus in children (P = 1.02e-04). Furthermore, the interactions significantly predict new-onset depression at a 2-year follow-up in children. Stunted increase in cortical thickness of the left middle-anterior cingulate gyrus and sulcus significantly mediates the interaction between childhood maltreatment and IDO2 on childhood depression. These interactions also moderate antidepressant treatment efficacy at 4-6 weeks.
科研通智能强力驱动
Strongly Powered by AbleSci AI