Aside from being teratogenic, ethanol is known to exert its effects in a stage-specific manner [48]. If we assume that human iPS cells model early embryonic development, and NPCs represent both early and adult neurogenesis stages, we can speculate that exposure of the human brain to ethanol at a very early phase of gestation, likely due to maternal drinking habits, can lead to a pathological impairment of postnatal neurogenesis, such as causing FASD. On the contrary, exposure of an adult human brain to ethanol (i.e. under AUDs) generates variable grades of neuronal dysfunction, depending on age, genetic and epigenetic backgrounds. As a matter of fact, previous data reported a temporal susceptibility to ethanol neurotoxicity during development [49–51]. In accordance with this, we have shown that iPS cells are more sensitive to oxidative damage than iPS cell-derived NPCs, and that these effects are strongly exacerbated by a prior exposure to ethanol.
