While the molecular basis receives attention, development of a molecular-based diagnosis is still in a deficit: understanding Attention Deficit Hyperactivity Disorder

Abstract

Attention deficit hyperactivity disorder is the most prevalent childhood-onset behavioral disorder, affecting approximately 8% of the population, where a disproportionate amount of males are afflicted. Common symptoms of the disorder include inattentiveness, hyperactivity, and impulsivity. Genomewide linkage analyses have demonstrated that the disorder is likely due to several genetic factors, whereby the dopaminergic, serotonergic, and noradrenergic neurotransmitter systems are highly implicated through various observations. Genetic screens of afflicted individuals have implicated the presence of specific genetic polymorphisms with ADHD, examples being the 10-repeat-40-base-pair allele of the dopamine transporter, DAT-1, and the silent-G861C-substitution allele of the serotonin receptor, 5-HT1B. Evidence is emerging that proteins involved in the release of neurotransmitters from synaptic vesicles, like SNAP-25, may also be involved in the pathology of ADHD. The most common method of treatment is the administration of psychostimulants, like amphetamine derivatives and methylphenidate (Ritalin®), drugs which target the dopaminergic system. New therapies that target other neurotransmitter systems, like the selective noradrenaline transport inhibitor, atomoxetine, are gaining recognition as effective treatments. Common methods to diagnose ADHD reside in psychological assessments. As more insight is gained into the genetic basis for the disorder, it appears likely that a clinical diagnostic test based on genetic screening for these factors, such as specific genetic polymorphisms, could serve as an additional means of diagnosis.