Attention-deficit/hyperactivity disorder (ADHD) symptoms typically emerge early in childhood and then either partially remit or persist during development. Approximately 30–50% of childhood cases remit by adolescence (Halperin, Trampush, Miller, Marks & Newcorn, 2008), and as many as 85% remit by the age of 25 years if full DSM-IV diagnostic criteria are applied (Faraone, Biederman & Mick, 2006). Nevertheless, most DSM-defined remitters remain symptomatic and many continue to have considerable impairment. Because of such marked diagnostic heterogeneity, it has been argued that ‘ADHD’ may be better conceptualized as representing the tail-end of a normally distributed cluster of dimensional traits that exist in the general population (Asherson, 2004). In support of this idea, at least one twin study has shown that genetic liability for ADHD is indeed continuously distributed throughout the general population (Chen, Zhou, Sham, Franke, Kuntsi, Campbell et al., 2008). Moreover, while childhood-onset ADHD is strongly heritable (Faraone, Perlis, Doyle, Smoller, Goralnick, Holmgren & Sklar, 2005), unique genetic factors seem to contribute to the stability of ADHD symptoms during development (Kuntsi, Rijsdijk, Ronald, Asherson & Plomin, 2005). However, specific genes that influence the developmental course of ADHD have not been identified.
