Catecholamine dysfunction is the main hypothesis to explain ADHD pathophysiology; specifically, the dysfunction in dopamine receptors D4, D5, and in dopamine transporter proteins (15, 41) in prefrontal cortex, nucleus accumbens, striatum, substantial nigra, ventral tegmentum, and frontal cortex (6). This evidence concerns the gene SLC6A3 and attention deficit-hyperactivity disorder.