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Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inappropriate levels of inattention, hyperactivity and impulsivity. Recent developments in neuroimaging and functional brain studies have revealed volumetric reductions and decreased neural activities in the frontal lobe, basal ganglia, limbic system, and cerebellum. Based on these findings, impairment of executive function and the reward system, reffered to as the dual pathway model, and dysfunction of the default mode network have been proposed as biological changes underlying ADHD. Bio-pharmacological studies have shown dysfunctions in catecholamine- regulated neurotransmission, especially dysfunction of dopamine transporters, which the therapeutic drug of methylphenidate is thought to modulate. Agrowing body of genetic research suggests the high heritability of ADHD and several candidate genes relating to dopamine synthesis and transmission have been identified. Epigenetic modification is also garnering much attention in ADHD research and the mutual effects of environmental factors and genetic polymorphism have been reported. Despite such accumulative findings, how genes, the environment, and brain functioning interact and relate to create the symptoms of ADHD are still unknown and more research is needed to uncover the biological mechanisms of ADHD.
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