AD/HD has a complex etiology, influenced by both genetic and environmental factors. Evidence for a strong genetic component is characterized by familial clustering, heritability estimated at 0.8, and support from twin and adoption studies (Albayrak et al., 2008). There have been numerous candidate gene association studies [reviewed in Ref. (Bobb et al., 2005)], a handful of genome-wide linkage studies (Fisher et al., 2002; Bakker et al., 2003; Arcos-Burgos et al., 2004; Hebebrand et al., 2006; Ogdie et al., 2006; Asherson et al., 2008; Romanos et al., 2008), and multiple whole-genome association studies published to date for AD/HD [reviewed in Ref. (Franke et al., 2009)]. Positive association signals in several candidate genes, including DAT1, DRD2, DRD4, DRD5, 5-HTT, 5-HT2A, and SNAP25, have been replicated in multiple studies, but none seem to have a large effect size (Wallis et al., 2008). There has also been limited success in identifying linkage regions that replicate across studies (Wallis et al., 2008). Thus, while much progress has been made in the field of AD/HD genetics it is clear that much remains to be investigated.
