2020/05/09 by Nina Kaminen‐Ahola · 78 citations
Biochemistry, Genetics and Molecular Biology · Medicine · #Allele #Bioinformatics #Biology #Birth, Development, and Health #Epigenetics #Epigenetics and DNA Methylation #Etiology #Fetal alcohol #Fetal alcohol syndrome #Gene #Genetics #Medicine #Pathology #Phenotype #Pregnancy #Prenatal Substance Exposure Effects #Prenatal alcohol exposure
paper · pdf · doi:10.1002/pd.5731
published in Prenatal Diagnosis 40(9), 1185-1192 (Wiley)
openalex publication_date 2020/05/09 · crossref created 2020/05/09 · crossref issued 2020/05/21 · crossref published 2020/05/21 · crossref published-online 2020/05/21 · crossref published-print 2020/08/01 · crossref deposited 2023/09/30 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29 · crossref indexed 2026/08/04
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.