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Published on: August 5, 2017
Epigenetics in fetal alcohol spectrum disorder
1Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States; Molecular Imaging and Neuropathology Area, New York State Psychiatric Institute, New York, New York, NY, United States; Department of Psychiatry, Columbia University Irving Medical Center, New York, NY, United States; Department of Psychiatry, New York University Langone Medical Center, New York, NY, United States.
Prenatal alcohol exposure causes fetal alcohol spectrum disorder (FASD) through epigenetic changes impacting gene expression. Understanding these epigenetic modifications offers potential therapeutic targets for FASD.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Alcohol (ethanol) abuse during pregnancy leads to fetal alcohol spectrum disorder (FASD), characterized by neurobehavioral impairments in offspring.
- FASD results from central nervous system (CNS) damage, causing structural and behavioral deficits.
Approach:
- Animal models are used to study FASD phenotypes and underlying mechanisms of prenatal ethanol exposure.
- Molecular approaches investigate immediate and enduring epigenetic modifications, including DNA methylation, histone post-translational modifications (PTMs), and RNA regulatory networks.
Key Points:
- Epigenetic factors, such as DNA methylation and histone PTMs, are implicated in the pathogenesis of FASD by disrupting gene expression.
- These epigenetic modifications are crucial for synaptic function and cognitive behavior, and their dysregulation contributes to FASD-related impairments.
- Recent advances highlight various epigenetic modifications contributing to FASD pathogenesis.
Conclusions:
- Understanding the role of epigenetic modifications in FASD is crucial for explaining its pathogenesis.
- This knowledge may pave the way for identifying novel therapeutic targets and developing innovative treatment strategies for FASD.
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