scholarly journals Prenatal Alcohol Exposure: Profiling Developmental DNA Methylation Patterns in Central and Peripheral Tissues

2018 ◽  
Vol 9 ◽  
Author(s):  
Alexandre A. Lussier ◽  
Tamara S. Bodnar ◽  
Matthew Mingay ◽  
Alexandre M. Morin ◽  
Martin Hirst ◽  
...  
Epigenomics ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 981-991 ◽  
Author(s):  
Yuk Jing Loke ◽  
Evelyne Muggli ◽  
Linh Nguyen ◽  
Joanne Ryan ◽  
Richard Saffery ◽  
...  

Alcohol ◽  
2011 ◽  
Vol 45 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Chris Downing ◽  
Thomas E. Johnson ◽  
Colin Larson ◽  
Tatiana I. Leakey ◽  
Rachel N. Siegfried ◽  
...  

Epigenomics ◽  
2015 ◽  
Vol 7 (8) ◽  
pp. 1259-1274 ◽  
Author(s):  
Benjamin I Laufer ◽  
Joachim Kapalanga ◽  
Christina A Castellani ◽  
Eric J Diehl ◽  
Liying Yan ◽  
...  

Epigenomics ◽  
2021 ◽  
Author(s):  
Yuk Jing Loke ◽  
Evelyne Muggli ◽  
Richard Saffery ◽  
Joanne Ryan ◽  
Sharon Lewis ◽  
...  

Background: Binge level prenatal alcohol exposure (PAE) causes developmental abnormalities, which may be mediated in part by epigenetic mechanisms. Despite this, few studies have characterised the association of binge PAE with DNA methylation in offspring. Methods: We investigated the association between binge PAE and genome-wide DNA methylation profiles in a sex-specific manner in neonatal buccal and placental samples. Results: We identified no differentially methylated CpGs or differentially methylated regions (DMRs) at false discovery rate <0.05. However, using a sum-of-ranks approach, we identified a DMR in each tissue of female offspring. The DMR identified in buccal samples is located near regions with previously-reported associations to fetal alcohol spectrum disorder (FASD) and binge PAE. Conclusion: Our findings warrant further replication and highlight a potential epigenetic link between binge PAE and FASD.


Genes ◽  
2021 ◽  
Vol 12 (11) ◽  
pp. 1773
Author(s):  
Alexandre A. Lussier ◽  
Tamara S. Bodnar ◽  
Michelle Moksa ◽  
Martin Hirst ◽  
Michael S. Kobor ◽  
...  

Prenatal adversity or stress can have long-term consequences on developmental trajectories and health outcomes. Although the biological mechanisms underlying these effects are poorly understood, epigenetic modifications, such as DNA methylation, have the potential to link early-life environments to alterations in physiological systems, with long-term functional implications. We investigated the consequences of two prenatal insults, prenatal alcohol exposure (PAE) and food-related stress, on DNA methylation profiles of the rat brain during early development. As these insults can have sex-specific effects on biological outcomes, we analyzed epigenome-wide DNA methylation patterns in prefrontal cortex, a key brain region involved in cognition, executive function, and behavior, of both males and females. We found sex-dependent and sex-concordant influences of these insults on epigenetic patterns. These alterations occurred in genes and pathways related to brain development and immune function, suggesting that PAE and food-related stress may reprogram neurobiological/physiological systems partly through central epigenetic changes, and may do so in a sex-dependent manner. Such epigenetic changes may reflect the sex-specific effects of prenatal insults on long-term functional and health outcomes and have important implications for understanding possible mechanisms underlying fetal alcohol spectrum disorder and other neurodevelopmental disorders.


2012 ◽  
Vol 13 (2) ◽  
pp. 32-42 ◽  
Author(s):  
Yvette D. Hyter

Abstract Complex trauma resulting from chronic maltreatment and prenatal alcohol exposure can significantly affect child development and academic outcomes. Children with histories of maltreatment and those with prenatal alcohol exposure exhibit remarkably similar central nervous system impairments. In this article, I will review the effects of each on the brain and discuss clinical implications for these populations of children.


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