Genomic endophenotypes of attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder (ADHD) is a remarkably heterogeneous neurobiological disorder. This characteristic is aetiologically mediated by genetic and environmental factors. Numerous studies have shown that different genes play a moderate but complex role in the aetiology of ADHD. Significant associations have been identified with several candidate genes for this disorder, including DAT1, DRD4, DRD5, 5HTT, HTR1B or SNAP25. The neurocognitive models of ADHD have been largely based on the findings from neuroimaging studies conducted in patients with ADHD, when establishing hypotheses capable of explaining the clinical features that are observed. From a neurobiological point of view, the genetic architecture of these patients or the interaction of the above-mentioned genes should at least partially account for the neuroanatomical and neuropsychological findings observed, which explains the axiomatic antithesis in the title. Nevertheless, the results of studies into the relationship between the genotyping and the neuroimaging or psychological findings are scarce and contradictory. The methodological differences in the volumetric analyses, the sizes of the populations studied, the neuropsychological batteries that are used, the presence of previous pharmacological treatment or comorbidity could account for these results.