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Published on: August 5, 2017
Fetal alcohol spectrum disorders and cognitive functions of young children
Insights
Fetal alcohol spectrum disorder (FASD), a leading cause of mental retardation, affects nearly 1% of North American children due to prenatal ethanol exposure. This review summarizes FASD
Area of Science:
- Neuroscience and Developmental Pediatrics
- Public Health and Epidemiology
Background:
- Fetal alcohol spectrum disorder (FASD) is a significant global cause of mental retardation, with North American prevalence around 1%.
- Antenatal ethanol exposure leads to FASD, imposing a substantial and increasing economic burden, estimated at $4.0 billion annually in the US for patient care.
- Fetal alcohol syndrome (FAS) is the most recognized clinical presentation, but FASD encompasses a broad range of cognitive and developmental impairments.
Purpose of the Study:
- To review the clinical manifestations of Fetal Alcohol Spectrum Disorder (FASD) in children and adolescents.
- To summarize the potential pathophysiologic and epigenetic mechanisms underlying FASD.
Main Methods:
- Review of scientific literature focusing on pretranslational and posttranslational factors implicated in FASD.
- Analysis of experimental animal models investigating the impact of antenatal ethanol exposure.
- Synthesis of research on neurotransmitters, HPA axis, insulin resistance, glycosylation, oxidative stress, and epigenetics.
Main Results:
- Extensive research over two decades has identified numerous factors contributing to FASD-related cognitive disorders.
- Key areas of investigation include neurotransmitter systems, hormonal regulation (HPA axis), metabolic pathways (insulin resistance), protein modification (glycosylation), and cellular stress (oxidative stress).
- Epigenetic factors are increasingly recognized as crucial in the pathophysiology of FASD.
Conclusions:
- FASD presents diverse clinical symptoms, with cognitive deficits being a primary concern.
- Multiple biological pathways, including neurobiological, metabolic, and epigenetic alterations, contribute to FASD.
- Further research into these pathways is essential for understanding and potentially mitigating the effects of prenatal ethanol exposure.
Abstract:
Fetal alcohol spectrum disorder (FASD) is one of the main causes of mental retardation worldwide. Nearly 1% of children in North America are affected from antenatal exposure to ethanol. Its economic burden in industrialized countries is increasing. It is estimated that, in the United States, 4.0 billion dollars are annually expended in the treatment and rehabilitation of these patients. As a pathologic entity, they present with a broad symptomatology. Fetal alcohol syndrome (FAS) is the most readily recognized clinical manifestation of these disorders. Various factors seem to contribute in the pathogenesis of FASD-related cognitive disorders. During the last 20 years, several potential pretranslational and posttranslational factors have been extensively studied in various experimental animal models. Research has specifically focused on several neurotransmitters, insulin resistance, alterations of the hypothalamic-pituitary-adrenal (HPA) axis, abnormal glycosylation of several proteins, oxidative stress, nutritional antioxidants, and various epigenetic factors. The purpose of the present review is to summarize the clinical manifestations of this disorder during childhood and adolescence and to summarize the possible pathophysiologic and epigenetic pathways that have been implicated in the pathophysiology of FASD.
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