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首页> 外文期刊>Communications Biology >Metabolomic and transcriptomic signatures of prenatal excessive methionine support nature rather than nurture in schizophrenia pathogenesis
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Metabolomic and transcriptomic signatures of prenatal excessive methionine support nature rather than nurture in schizophrenia pathogenesis

机译：产前过量蛋氨酸的代谢组和转录组特征，而不是精神分裂症发病机制的培养

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The imbalance of prenatal micronutrients may perturb one-carbon (C1) metabolism and increase the risk for neuropsychiatric disorders. Prenatal excessive methionine (MET) produces in mice behavioral phenotypes reminiscent of human schizophrenia. Whether in-utero programming or early life caregiving mediate these effects is, however, unknown. Here, we show that the behavioral deficits of MET are independent of the early life mother-infant interaction. We also show that MET produces in early life profound changes in the brain C1 pathway components as well as glutamate transmission, mitochondrial function, and lipid metabolism. Bioinformatics analysis integrating metabolomics and transcriptomic data reveal dysregulations of glutamate transmission and lipid metabolism, and identify perturbed pathways of methylation and redox reactions. Our transcriptomics Linkage analysis of MET mice and schizophrenia subjects reveals master genes involved in inflammation and myelination. Finally, we identify potential metabolites as early biomarkers for neurodevelopmental defects and suggest therapeutic targets for schizophrenia. Chen, Alhassen et al. show that schizophrenia-like behavioral deficits induced by excessive prenatal methionine administration are due to in-uterus aberrations rather than through early life mother-infant interaction in mice. This study identifies the brain metabolites and transcriptomic signatures, which potentially serve as early biomarkers for schizophrenia-like behaviors.
机译：产前微量营养素的不平衡可能会扰动单碳（C1）代谢并增加神经精神疾病的风险。产前过量的蛋氨酸（Met）产生小鼠的行为表型让人让人感受到人体精神分裂症。然而，无论是Utero编程还是早期生活都介导这些效果，也是未知的。在这里，我们认为满足的行为赤字与早期生活母婴相互作用无关。我们还表明，在脑C1途径部件以及谷氨酸透射，线粒体功能和脂质代谢中产生的早期寿命深刻变化。生物信息学分析整合代谢组和转录组数据显示谷氨酸透射和脂质代谢的疑难解失用，鉴定甲基化和氧化还原反应的扰动途径。我们的转录组织联系对小鼠和精神分裂症受试者的联系分析揭示了患有炎症和髓鞘的母基因。最后，我们将潜在的代谢产物识别为早期生物标志物，用于神经开发缺陷，并表明精神分裂症治疗靶标。陈，阿尔哈什等人。表明，过量产前蛋氨酸给药诱导的精神分裂症的行为缺陷是由于子宫内像比而不是小鼠的早期母婴相互作用。该研究鉴定了脑代谢物和转录组织群，其可能作为精神分裂症类似的早期生物标志物。

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