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Published on: February 11, 2020
Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention
Shao-Yu Chen1, Maharajan Kannan1
1Department of Pharmacology and Toxicology, University of Louisville Health Sciences Center, Louisville, KY 40292, USA; University of Louisville Alcohol Research Center, Louisville, KY 40292, USA.
Insights
Prenatal alcohol exposure harms neural crest cells (NCCs), leading to fetal alcohol spectrum disorders (FASD). Understanding ethanol
Area of Science:
- Developmental Biology
- Neuroscience
- Teratology
Background:
- Fetal alcohol spectrum disorders (FASD) are preventable birth defects from prenatal alcohol exposure.
- Neural crest cells (NCCs) are crucial for developing the nervous system and craniofacial structures.
- Ethanol exposure during embryogenesis disrupts NCC development, causing FASD-related abnormalities.
Purpose of the Study:
- To review the detrimental effects of ethanol on NCC induction, migration, differentiation, and survival.
- To examine molecular mechanisms underlying ethanol-induced NCC dysfunction.
- To highlight potential therapeutic strategies for mitigating ethanol's impact on NCCs and FASD.
Main Methods:
- Literature review of existing research on ethanol's effects on NCCs.
- Analysis of molecular pathways involved in ethanol-induced NCC dysfunction.
- Synthesis of current knowledge on FASD pathogenesis related to NCCs.
Main Results:
- Ethanol exposure significantly impairs NCC induction, migration, differentiation, and survival.
- Molecular mechanisms include oxidative stress, altered gene expression, apoptosis, and epigenetic changes.
- These disruptions in NCCs contribute to the diverse structural and functional deficits seen in FASD.
Conclusions:
- Ethanol's adverse effects on NCCs are a key factor in FASD development.
- Targeting molecular pathways affected by ethanol may offer therapeutic interventions.
- Further research is needed to develop effective strategies for preventing and treating FASD.
Abstract:
Fetal alcohol spectrum disorders (FASD) are a group of preventable and nongenetic birth defects caused by prenatal alcohol exposure that can result in a range of cognitive, behavioral, emotional, and functioning deficits, as well as craniofacial dysmorphology and other congenital defects. During embryonic development, neural crest cells (NCCs) play a critical role in giving rise to many cell types in the developing embryos, including those in the peripheral nervous system and craniofacial structures. Ethanol exposure during this critical period can have detrimental effects on NCC induction, migration, differentiation, and survival, leading to a broad range of structural and functional abnormalities observed in individuals with FASD. This review article provides an overview of the current knowledge on the detrimental effects of ethanol on NCC induction, migration, differentiation, and survival. The article also examines the molecular mechanisms involved in ethanol-induced NCC dysfunction, such as oxidative stress, altered gene expression, apoptosis, epigenetic modifications, and other signaling pathways. Furthermore, the review highlights potential therapeutic strategies for preventing or mitigating the detrimental effects of ethanol on NCCs and reducing the risk of FASD. Overall, this article offers a comprehensive overview of the current understanding of the impact of ethanol on NCCs and its role in FASD, shedding light on potential avenues for future research and intervention.
