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DNA methylation plays a key role in neural cell fate and provides a molecular link between early life stress and later-life behavioral phenotypes. Here, studies that combine neuroimaging methods and DNA methylation analysis in pediatric population with a history of adverse experiences were systematically reviewed focusing on: targeted genes and neural correlates; statistical models used to examine the link between DNA methylation and neuroimaging data also considering early life stress and behavioral outcomes. We identified 8 studies that report associations between DNA methylation and brain structure/functions in infants, school age children and adolescents faced with early life stress condition (e.g., preterm birth, childhood maltreatment, low socioeconomic status, and less-than optimal caregiving). Results showed that several genes were investigated (e.g., OXTR, SLC6A4, FKBP5, and BDNF) and different neuroimaging techniques were performed (MRI and f-NIRS). Statistical model used ranged from correlational to more complex moderated mediation models. Most of the studies (n = 5) considered DNA methylation and neural correlates as mediators in the relationship between early life stress and behavioral phenotypes. Understanding what role DNA methylation and neural correlates play in interaction with early life stress and behavioral outcomes is crucial to promote theory-driven studies as the future direction of this research fields.

DNA methylation plays a key role in neural cell fate and provides a molecular link between early life stress and later-life behavioral phenotypes. Here, studies that combine neuroimaging methods and DNA methylation analysis in pediatric population with a history of adverse experiences were systematically reviewed focusing on: targeted genes and neural correlates; statistical models used to examine the link between DNA methylation and neuroimaging data also considering early life stress and behavioral outcomes. We identified 8 studies that report associations between DNA methylation and brain structure/functions in infants, school age children and adolescents faced with early life stress condition (e.g., preterm birth, childhood maltreatment, low socioeconomic status, and less-than optimal caregiving). Results showed that several genes were investigated (e.g., OXTR , SLC6A4 , FKBP5 , and BDNF) and different neuroimaging techniques were performed (MRI and f -NIRS). Statistical model used ranged from correlational to more complex moderated mediation models. Most of the studies (n = 5) considered DNA methylation and neural correlates as mediators in the relationship between early life stress and behavioral phenotypes. Understanding what role DNA methylation and neural correlates play in interaction with early life stress and behavioral outcomes is crucial to promote theory-driven studies as the future direction of this research fields. [ABSTRACT FROM AUTHOR]

Oxytocin has anxiolytic properties whose mechanisms of action are still being identified. DNA methylation in the promoter region of the oxytocin receptor gene (OXTR), an epigenetic modification that putatively reflects a downtuning of the oxytocin system, has previously been implicated in the regulation of fear-related responses through the amygdala. In this study, we attempted to characterize the relationship between methylation of OXTR and anxiogenesis using two distinct endophenotypes: autonomic nervous system activity and subcortical brain structure. In 79 participants, we found that increased OXTR methylation is associated with attenuated resting parasympathetic tone, measured using high-frequency heart rate variability. Further, we found that this relationship is mediated by brain morphology, such that OXTR methylation is associated with increased gray matter of the central amygdala which is, in turn, associated with decreased parasympathetic tone. These results further our understanding of epigenetic regulation of the human oxytocin system and its role in anxiogenesis. [ABSTRACT FROM AUTHOR]