Identifying the individual genes contributing to the genetic variance of ADHD has proven difficult. Two approaches have been available for this type of research until recently: hypothesis-driven candidate gene association studies and hypothesis-free genome-wide linkage analysis. Although hundreds of candidate gene studies have been reported (see for example Bobb et al. 2005; Khan and Faraone 2006), only a handful of associations have been replicated across studies, although none of these achieved genome-wide significance (e.g. Faraone et al. 2005; Li et al. 2006). These studies have mainly concentrated on genes involved in neurotransmission, particularly in the catecholaminergic systems involved in the response to ADHD medications. Clearly, the hypothesis-driven approach has been limited by our restricted knowledge regarding mechanisms involved in ADHD pathogenesis. Genome-wide, hypothesis-free linkage analysis has been performed in ADHD using qualitative and quantitative definitions of the disease phenotype (Arcos-Burgos et al. 2004; Asherson et al. 2008; Bakker et al. 2003; Hebebrand et al. 2006; Ogdie et al. 2003; Ogdie et al. 2004; Ogdie et al. 2006; Romanos et al. 2008; Zhou et al. 2008a), and recently also using ADHD
