This study examined whether changes in working memory maintenance and manipulation differentially correlated with the stability of ADHD symptoms over a 10-year period as a function of DRD1 and DRD2 polymorphisms in a prospectively followed sample of youth with childhood-diagnosed ADHD. We reasoned that searching for a main effect of genotype on cognition and/or symptoms would yield an incomplete story; therefore, our analytical strategy incorporated higher-order interactions of genotype × cognition on clinical symptoms and development in the context of a targeted neurobiologic system important for working memory. We did not posit differential improvements in working memory based solely on dopamine receptor genotype, but rather we hypothesized that improvements in working memory would be linked to fewer symptoms over time depending on genetic background and developmental stage. The motivation to carry out this study was based on the aforementioned cumulative evidence showing links between (i) symptom recovery in ADHD and working memory during later development (Halperin et al., 2008), (ii) dopamine D1 receptors in the prefrontal cortex being critical to working memory (Paspalas & Goldman-Rakic, 2005), and (iii) the prefrontal
