Another important aspect of stress and alcohol overlap is the dynamic nature of epigenetic alterations to Bdnf. In animal models of both FASD and early-life stress the implications of teratogen exposure on the epigenome can vary depending upon age. For example, in an animal model of FASD methylation of Bdnf exon I was reduced on PD10, but methylation levels normalized by PD72 (Boschen et al., 2015; Boschen et al., 2016). A similar effect was observed in an animal model of early-life stress, where Bdnf exon IV methylation was reduced in the adolescent brain but increased in the adult brain (Blaze et al., 2013). The significance of the dynamic nature of these epigenetic changes remains to be elucidated. Learning and memory processes and normal neural development rely on ever-changing patterns of epigenetic marks, thus it is important to put any epigenetic modifications in the context of normative epigenetic programming and gene activity (Meaney and Ferguson-Smith, 2010; Szulwach et al., 2011). In addition, disruptions to neural development arising from aberrant epigenetic programming early in life could predispose an individual to developing neuropsychiatric disorders in adulthood, even if the epigenetic patterns normalize over time (Ptak and Petronis, 2010).
