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Fetal alcohol spectrum disorder
Abstract
This chapter provides an overview of animal model-based studies that have generated information critical to our understanding of the pathogenesis and mechanisms underlying alcohol-induced birth defects, in particular those involving the brain. Focus is placed on the developing organism itself, rather than the mother, placenta, or other extraembryonic tissues. Components of the cascades of alcohol-induced damage that are considered herein are excessive cell death, changes in the cell cycle and proliferation, cell migration, cell morphogenesis, and gene expression as well as free radical damage and interference with cell signaling. The roles played by one or more of these various factors in the genesis of structural and functional birth defects are dependent upon alcohol exposure patterns and dosage, the involved tissue, and the prenatal stage(s) at the time of exposure. Technologic advances and rapidly increasing knowledge in the fields of genetics, cell, developmental, and neurobiology are critical to accurately piecing together experimental evidence in refining our understanding of the genesis of alcohol-induced birth defects, to the planning and execution of future studies, and to applying the knowledge gained to diminish the severity or occurrence of fetal alcohol spectrum disorder.
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The type and severity of ethanol-induced birth defects are dependent largely upon the pattern, dose and developmental stage of the embryo at the time of ethanol exposure.
“While human research has not delineated, and perhaps cannot delineate fully, the pattern, amount and/or critical period of alcohol exposure necessary for structural and/or functional teratogenesis, animal models have shown that all stages of embryonic development are vulnerable to the teratogenic effects of ethanol, and that the type and severity of ethanol‐induced birth defects are dependent larg”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [63]
Animal models have shown that all stages of embryonic development are vulnerable to the teratogenic effects of ethanol.
“While human research has not delineated, and perhaps cannot delineate fully, the pattern, amount and/or critical period of alcohol exposure necessary for structural and/or functional teratogenesis, animal models have shown that all stages of embryonic development are vulnerable to the teratogenic effects of ethanol, and that the type and severity of ethanol‐induced birth defects are dependent larg”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [63]
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Alternating metabolic pathways in NGF-deprived sympathetic neurons affect caspase-independent death
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Ethanol Alters BDNF-Induced Rho GTPase Activation in Axonal Growth Cones
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Ethanol Antagonist Peptides: Structural Specificity without Stereospecificity
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Concurrent Dietary Administration of D‐SAL and Ethanol Diminishes Ethanol’s Teratogenesis
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Metadata
- Authors
- Sulik, K. K.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Kathleen K. Sulik
- Venue
- Handbook of Clinical Neurology
- Publisher
- Elsevier
- Published
- 2014
- Volume
- 125
- Pages
- 463-475
- ISSN
- 0072-9752 (ISSN-L)
- OpenAlex
- W202227517
- Cited by
- 45
- References
- 129
- Citations by year
- 2026: 2 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 1 · 2020: 6 · 2019: 5 · 2018: 4 · 2017: 10 · 2016: 6 · 2015: 1
- FWCI
- 43.40
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Handbook of clinical neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Fetal and Pediatric Neurological Disorders
- Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
- Keywords
- fetal alcohol spectrum disorders, prenatal alcohol exposure, animal models, brain development, cell death, cell cycle, cell proliferation, cell migration, morphogenesis, gene expression, oxidative damage, signal transduction, developmental neuroscience, pathogenesis
- MeSH terms
- Alcohol Drinking, Animals, Brain, Cell Movement, Female, Humans, Pregnancy, Prenatal Exposure Delayed Effects, Cell Death, Epigenesis, Genetic, Fetal Alcohol Spectrum Disorders
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