ABSTRACT
Twin, family, and adoption studies provide compelling evidence that genetic risk factors contribute substantially to attention deficit hyperactivity disorder (ADHD) (1,2). Twin studies show high genetic contribution regardless of whether ADHD is defined as a category, as a continuous trait, or as an extreme of a trait (h2¼ .64 to .9) (3,4). Genetic linkage and association studies have proven remarkably productive in ADHD identifying a number of genetic risks for the disorder (3). Progress in ADHD was swift because scientists were forearmed with considerable knowledge about the probable role of neurotransmitter dysfunction based on the dramatic effect of stimulant medication in ameliorating behavioral and cognitive manifestations of ADHD (5,6). There have now been over 30 association reports for candidate genes including the genes for the DA transporter (DAT1), DA receptors D4 and D5, the serotonin receptors 1B and 2A, calcyon, EKN1, G(olf), and the gene for the synaptic vesicle docking fusion protein, synaptosomal-associated protein of 25 kDa (SNAP25) (3,7). Furthermore, there have been four genome wide scans on relatively small, independent samples (8-11), which are suggestive of linkage signals in the distal region of chromosome 5p.
