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Published on: July 13, 2014
Impact of Prenatal Alcohol Exposure on the Cerebral Circulation: Potential Implications for Stroke
Partha S Saha1, Denise M Arrick2, William G Mayhan3
1School of Science, Technology, Engineering, and Math (STEM), Diné College, Shiprock, NM, USA.
Insights
Prenatal alcohol exposure (PAE) harms neural and vascular development, causing fetal alcohol spectrum disorder (FASD). Understanding these effects is key to developing therapies for affected children and adults.
Area of Science:
- Neuroscience
- Developmental Biology
- Teratology
Background:
- Prenatal alcohol exposure (PAE) is a significant teratogenic factor impacting fetal development.
- PAE leads to structural, functional, and cognitive/behavioral abnormalities, contributing to fetal alcohol spectrum disorder (FASD).
- FASD is a leading preventable cause of human developmental delay.
Purpose of the Study:
- To review the impact of PAE on neural and vascular development and function.
- To identify potential cellular and molecular mechanisms underlying PAE's effects.
- To explore how understanding PAE's influence on cerebral vasculature can illuminate FASD pathogenesis.
Main Methods:
- Literature review focusing on PAE's effects on neurodevelopment and cerebrovascular systems.
- Analysis of molecular and cellular mechanisms implicated in PAE-induced abnormalities.
- Synthesis of current research to connect vascular function to FASD symptoms.
Main Results:
- PAE significantly disrupts normal neural development pathways.
- Alterations in cerebral vascular development and function are critical consequences of PAE.
- Specific molecular and cellular mechanisms link PAE to FASD-related deficits.
Conclusions:
- Understanding PAE's impact on neural and vascular systems is crucial for therapeutic development.
- Cerebral vascular dysfunction is a key factor in FASD pathogenesis.
- Targeting PAE-induced vascular effects may offer novel therapeutic strategies for FASD.
Abstract:
Prenatal alcohol exposure (PAE) is recognized as a teratogenic factor that affects neural development, resulting in a range of structural, functional, and cognitive/behavioral abnormalities contributing to the pathogenesis of fetal alcohol spectrum disorder (FASD). FASD is a major preventable cause of developmental delay in humans. There are many molecular and cellular mechanisms by which PAE could contribute to abnormalities seen in individuals with FASD. Understanding these mechanisms will be critical for the development of therapeutic approaches that could benefit not only the developing fetus, but the newborn as they mature into adolescence and adulthood. The goal of this review is to discuss the impact of PAE on neural and vascular development/function and define potential cellular/molecular mechanisms that contribute to the effects of PAE. We believe that an understanding regarding the influence of PAE on cerebral vascular function may provide insights into the pathogenesis of symptoms related to FASD.
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