Adv Exp Med Biol. 2026;1500:27-48. doi: 10.1007/978-3-032-12741-9_2.
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.
PMID:41478917 | DOI:10.1007/978-3-032-12741-9_2