Since FAS was first described, more than 25 years ago, the molecular and cellular mechanisms through which PEA is thought to exert its detrimental effects on the developing brain have been slowly elucidated, with significant progress made over the last decade. Initial findings highlighted the regional vulnerability of specific brain structures, including the neocortex, cerebellum and hippocampus, to ethanol-induced neuronal cell loss128, 129. Subsequently, researchers determined that prenatal alcohol exposure alters maturation of glial cells130, and that this is associated with failure of neuroblasts to migrate to their proper targets131, suggesting that alcohol-induced impairment of neurogenesis and neuronal migration contribute to alterations in brain size and cortical architecture. More recent studies have emphasized the relevance of alcohol-induced cell necrosis and enhanced natural apoptosis, mediated by glutamatergic antagonism at the NMDA receptor and GABA-mimetic actions at the GABA-A receptor132. Additionally, a number of other factors have been implicated as potential contributors to the neurotoxicity of prenatal alcohol, including nutritional133 and socioeconomic factors134, genetic susceptibility linked to polymorphisms in alcohol and aldehyde dehydrogenase, and the serotonin transporter gene promoter (5-HTTLPR)135, alcohol-induced hypoxia136,
