title: Current concepts on the neurobiology of Attention-Deficit/Hyperactivity Disorder.
abstract: Attention-Deficit/Hyperactivity Disorder (ADHD) is an early onset, clinically heterogeneous disorder of inattention, hyperactivity, and impulsivity. In contrast to the widespread acceptance of ADHD as a childhood diagnosis, Its prevalence In adults and its implications for clinical practice remain a source of controversy. Throughout the lifecycle, a key clinical feature observed in ADHD patients is comorbidity with Conduct Depressive, Bipolar, and Anxiety disorders. Family studies consistently support the assertion that ADHD runs in families. Heritability data from twin studies of ADHD attribute about 80 percent of the etiology of ADHD to genetic factors. Adoption studies of ADHD also implicate genes in its etiology. Molecular genetic data are bolstered by considerations suggesting that DRD4 and DAT genes may be relevant for ADHD. Independently of genes, prenatal exposure to nicotine and psychosocial adversity have also been identified as risk factors for ADHD. Structural and functional imaging studies consistently implicate catecholamine-rich fronto-subcortical systems in the pathophysiology of ADHD. The effectiveness of stimulants, along with animal models of hyperactivity, point to catecholamine disruption as at least one source of ADHD brain dysfunction. Although not entirely sufficient, changes in dopaminergic and noradrenergic function appear necessary for the clinical efficacy of pharmacological treatments for ADHD, providing support for the hypothesis that alteration of monoaminergic transmission in critical brain regions may be the basis for therapeutic action in ADHD.
authors.affiliation: Pediatric Psychopharmacology Unit of the Child Psychiatry Service, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA.
authors.forename: J
authors.initials: J
authors.lastname: Biederman
authors.forename: S V
authors.initials: SV
authors.lastname: Faraone
mesh_terms: D000328:Adult; D001289:Attention Deficit Disorder with Hyperactivity / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology*; D001921:Brain / Q000503:physiopathology*; D001931:Brain Mapping; D002395:Catecholamines / Q000502:physiology*; D002648:Child; D015897:Comorbidity; D050483:Dopamine Plasma Membrane Transport Proteins; D005625:Frontal Lobe / Q000503:physiopathology*; D006801:Humans; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins / Q000235:genetics / Q000502:physiology; D001523:Mental Disorders / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology; D009419:Nerve Tissue Proteins; D017448:Receptors, Dopamine D2 / Q000235:genetics / Q000502:physiology; D050638:Receptors, Dopamine D4; D012307:Risk Factors; D018433:Twin Studies as Topic
chemical_list: D002395:Catecholamines; C493599:DRD4 protein, human; D050483:Dopamine Plasma Membrane Transport Proteins; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D009419:Nerve Tissue Proteins; D017448:Receptors, Dopamine D2; C493214:SLC6A3 protein, human; D050638:Receptors, Dopamine D4