disorders. Clustered protocadherin genes were differentially methylated in this sample, similar to previous human and animal work (Chater-Diehl et al., 2016; Laufer et al., 2015). A factor limiting interpretation of these data is the relatively low increase in methylation (>5%) and its relation to gene expression changes in the FASD population. It is worth noting that similarly sized effects were reported in postmortem brain tissue from individuals with autism (Ladd-Acosta et al., 2014). In addition, both the FASD and autistic samples were possibly confounded by the influence of environmental factors, as the mean age of the FASD sample was ~11 years old and ~21 years old in the autistic sample. It is possible that environmental influences could have removed epigenetic marks or created new ones. While more work needs to be done to fully understand the implications of this data, these data suggest that methylation patterns in children with FASD could contribute to long-term cognitive and behavioral outcomes and interventions that affect the epigenome should be explored as therapeutic agents.
