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, alcohol-induced free radical production137 and inhibition of cell adhesion mediated by the human L1 gene138. How these potential mechanisms contribute individually and collectively to altered brain growth and maturation resulting from alcohol exposure has so far not been clearly established, and additional mechanisms may be operative with specific developmental consequences (for review, see Guerri139). The subsequent paragraphs briefly review the neuroimaging literature in subjects with PEA.
