Interference of cellular metabolism and differentiation as a result of epigenetic disruption is a major consequence of alcohol exposure (De Filippis et al., 2016). Progression of neurological disorders initiated by alcohol abuse are exacerbated by neuroinflammation and oxidative damage of cellular proteins and mitochondria (Haorah et al., 2008). The ability for alcohol to initiate an innate immune-like response was investigated in the CNS using patient derived iPS cells, to generate neural cell types specific to the same individual (De Filippis et al., 2016). Pathogenesis of AUDs were modeled in such way that allowed the researchers to study alcohol’s effects on pluripotency (iPS cells), neurogenesis (neural progenitor cells, NPCs) and differentiation (post-mitotic neurons) (De Filippis et al., 2016).
