Consistent with the dimensional approach to studying ADHD, the quantitative trait locus model typically used in gene mapping studies assumes that the genetic variance (captured by the heritability estimates from twin studies) in ADHD symptoms is likely to be accounted for by multiple genetic variants, each conferring a relatively small risk for disease (or trait) susceptibility.8–10 A recent meta-analysis concluded that significant associations could be identified only for the dopamine transporter gene (DAT1), D4 and D5 receptor genes, the serotonin transporter and receptor genes, and the synaptosomal-associated protein 25 gene.11 Although findings across genetic association studies of ADHD (as with all psychiatric disorders) remain inconsistent, one clear conclusion does emerge: the estimated effect sizes of individual genetic variants are small, with odds ratios in the range of 1.12 to 1.33.11 Very large samples within powerful designs will be needed to detect odds ratios of this magnitude, given the observed minor allele frequencies for current ADHD-risk alleles. Genome-wide association studies (GWAS), in which “a dense set of SNPs [single nucleotide polymorphisms] across the genome is genotyped to survey the most common
