treated cells. Thus, we suggest that an ethanol-mediated pro-apoptotic pathway additionally includes the participation of a disturbed autophagy process. Interestingly, it’s known that the inflammasome and autophagy pathways may participate independently of ethanol-mediated responses [43, 44]. However, given the multiplicity of pathways involved in both the regulation of autophagy and of the inflammasome, further studies will be necessary to dissect the different mechanisms engaged by ethanol-driven neuropathology. Along with the activation of the inflammasome pathway, an impaired elimination of defective mitochondria by selective autophagy (mitophagy) is among the most likely mediators of ethanol-induced damage [5, 9, 17]. Indeed, ethanol is known to cause damage to mitochondria resulting in the production of intracellular reactive oxygen species [4, 45, 46]. We found that mitochondrial distribution was altered in both iPS cells and NPCs, with a reduction in mitochondrial content, as well as an increased tendency to cluster in treated versus untreated cells. Nevertheless, no specific differences were detectable between the acute (24hr) or prolonged (7d) exposure [21, 32, 47]. Our findings suggest that even a very transient exposure to ethanol (24hr) will make both iPS cells and NPCs more sensitive to oxidative damage, resulting in a shift from a physiological homeostatic metabolism
