Generally, the results of both candidate gene-based association studies and genome-wide linkage studies have not identified major genes for ADHD. In candidate gene studies, individual gene variants have only shown small effects, rarely reaching an odds ratio of 1.3 (e.g. Faraone et al. 2005). This strongly limits the power of genetic linkage designs in ADHD research, as these designs are suited for the identification of individual genetic variants that explain at least 10% of the genetic variance of a trait or disease (Risch and Merikangas 1996). A situation like this calls for a new analytic approach, one which combines the power to detect genetic variants of small effect size, like the association studies, with the possibility to perform hypothesis-free analyses of the entire genome. This has recently become feasible using the genome-wide association study (GWAS) methodology. In GWAS, 100,000 to more than 1,000,000 genetic variants (in this case single nucleotide polymorphisms, SNPs), distributed across the entire genome are genotyped using a microarray platform and (individually) tested for association with a trait or disorder. The selection of SNPs is mostly based
