One of the most important aspects of these data is the developmental component and the examination of phenotypic change and variability over a decade. Our results suggest that the genetic factors that contribute to the emergence of ADHD in early childhood may not be the same factors that contribute to its course and outcome throughout adolescence and adulthood (Kuntsi et al., 2005). Our sample was initially recruited between the ages of 7 and 11, the approximate age range that the preponderance of molecular genetic studies of ADHD have likewise utilized (Faraone et al., 2005), with dopamine being the most extensively studied neurotransmitter system in this age group. Because the maturation of the anatomy and physiology of dopamine in general, and D1 receptor expression specifically in the cortex, is slower than other regions of the brain (Andersen et al., 2000), we did not expect to find significant dopamine gene effects at baseline and so focused on the developmental course of working memory and ADHD symptoms. For that reason, it is not surprising that dopamine gene associations with ADHD are difficult to
