The placenta as a window to the brain: A review on the role of placental markers in prenatal programming of neurodevelopment

表观遗传学 胎盘 胎儿 神经科学 产前应激 生物信息学 后生 机会之窗 怀孕 生物 心理学 DNA甲基化 基因表达 基因 后代 遗传学 实时计算 计算机科学
作者
Philemon Shallie,Thajasvarie Naicker
出处
期刊:International Journal of Developmental Neuroscience [Wiley]
卷期号:73 (1): 41-49 被引量:83
标识
DOI:10.1016/j.ijdevneu.2019.01.003
摘要

Abstract Background During development, the placenta can be said to be the most important organ, however, the most poorly researched. There is currently a broader understanding of how specific insults during development affect the fetal brain, and also the importance of placental signaling in neurodevelopmental programming. Epigenetic responses to maternal and fetal signals are an obvious candidate for transforming early life inputs into long‐term programmatic outcomes. As a mediator of maternal and environmental signals to the developing fetus, epigenetic processes within the placenta are particularly powerful such that alterations of placental gene expression, downstream function, and signalling during foetal development have the potential for dramatic changes in developmental programming. Summary In this article, we reviewed emerging evidence for a placental role in prenatal neurodevelopmental programming with a specific focus on nutrient and prenatal stress signals integration into chromatin changes; this new understanding, we hope will provide the means for lowering developmentally based disorder risk, and new therapeutic targets for treatment in adulthood. Key messages Based on this review, the placenta is a potent micro‐environmental player in neurodevelopment as it orchestrates a series of complex maternal–foetal interactions. Maternal insults to this microenvironment will impair these processes and disrupt foetal brain development resulting in the prenatal programming of neurodevelopmental disorders. These findings should inspire advance animal model and human research drive to appraise gene–environment impacts during pregnancy that will target the developmental cause of adult‐onset mental disorders.

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