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Fetal alcohol spectrum disorders (FASD) are a consequence of prenatal alcohol exposure (PAE). The etiology of the complex FASD phenotype with growth deficit, birth defects, and neurodevelopmental impairments is under extensive research. Both genetic and environmental factors contribute to the wide phenotype: chromosomal rearrangements, risk and protective alleles, environmental‐induced epigenetic alterations as well as gene‐environment interactions are all involved. Understanding the molecular mechanisms of PAE can provide tools for prevention or intervention of the alcohol‐induced developmental disorders in the future. By revealing the alcohol‐induced genetic and epigenetic alterations which associate with the variable FASD phenotypes, it is possible to identify biomarkers for the disorder. This would enable early diagnoses and personalized support for development of the affected child.