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NR2F1 IS A CROSS-SPECIES MEDIATOR OF CEREBRAL CORTEX DEFECTS INDUCED BY FETAL ALCOHOL INTOXICATION
Manon Charletand 21 co-authors
University of Liège
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-093
Presentation
Date TBA
Board: PS01-07AM-093
Event Information
Poster Board
PS01-07AM-093
Poster
View posterAbstract
Prenatal alcohol exposure (PAE) causes a spectrum of neurodevelopmental disorders collectively termed Fetal Alcohol Spectrum Disorders. Using a voluntary maternal alcohol consumption model in mice, here we show that PAE disrupts the migration and connectivity of callosal projection neurons in the developing somatosensory cortex. Mechanistically, PAE induces upregulation of NR2F1, together with downregulation of its direct targets Lis1 and Kif1b, essential for neuronal migration and differentiation. These molecular alterations are conserved in the developing cortex of human fetuses with documented prenatal alcohol exposure as well as in human cerebral organoids engrafted into mice exposed to ethanol. Our findings reveal a conserved molecular and cellular pathway disrupted by prenatal alcohol exposure (PAE), highlighting NR2F1 as a key regulator in the pathogenesis of fetal alcohol spectrum disorders (FASD) and suggesting new avenues for therapeutic intervention targeting alcohol-induced neurodevelopmental impairments.
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