been strongly focused on childhood. The age of onset for ASD and ADHD is nearly always in childhood ([18]; but see [17]), which is the likely reason for this bias. However, given that it is already well known that developmental changes take place in both ADHD and ASD symptom domains separately, a focus beyond childhood is needed to further understand the potentially changing etiology of ADHD-ASD co-occurrence.
Heritability of ADHD across the lifespanSeveral longitudinal twin studies on ADHD symptoms report that new, age-specific genetic effects influence ADHD symptoms in adolescence and adulthood, suggesting that ADHD symptoms are a developmentally complex phenotype characterized by both continuity and change across the life span [3,9,12,13,19]. In addition, only a modest overlap between longitudinal genetic effects underlying both symptom domains (inattention versus hyperactivity/impulsivity) appears present, suggesting it is necessary to study both separately. Moreover, several longitudinal studies report that subgroups may be formed based on various combinations of symptoms in both domains across the longitudinal course that likely has partly distinct genetic underpinnings ([7, 14, 25]). These findings strongly suggest that genetic effects implicated in childhood ADHD may not at all be directly comparable to those that influence ADHD in adulthood. This concurs with a review on molecular genetics in adult ADHD, where it was concluded that only some genes potentially related to childhood ADHD have been replicated in adults with the disorder [8]. In addition, in some cases the same genes were implicated, but different alleles increased the risk for ADHD in children versus adults (for instance, the 10-repeat in the dopamine transporter gene [DAT1] increased the risk for ADHD in children, but decreased the risk in adults) [8]. Note though that currently