New Genetic Findings In Attention Deficit Hyperactivity

March 19, 1999

Mapping susceptibility loci in attention deficit hyperactivity disorder: Preferential transmission of parental alleles at DAT1, DBH and DRD5 to affected children.

Attention Deficit Hyperactivity Disorder (ADHD) is a disorder of childhood characterized by inattention, excessive motor activity, impulsivity, and distractibility, affecting between 4% and 6% of the school-age population. ADHD is familial and twin studies estimate heritibility (h2) at 80-90%. The mode of transmission is unknown, but is likely to be due to many genes, each of small effect. The increased risk in 1st degree relatives is 5-6, suggesting that relative risks at individual loci will be small. Pharmacological and biochemical studies have suggested that dopaminergic and nor-adrenergic systems are involved. Using a sample of affected children and their parents the authors have found preferential transmission of alleles at polymorphisms at the Dopamine transporter gene (DAT1), Dopamine-b-hydroxylase (DBH) and the Dopamine D5 receptor (DRD5). The DAT1 results re-confirm and extend their previous findings for this polymorphism. Transmission of the 'associated' alleles at DAT1 and DBH is stronger in familial cases, but for DRD5, transmission is stronger in non-familial cases. Attributable fractions for DAT1, DBH and DRD5 are calculated at .08, .12 and .20 respectively.
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For further information on this work, please contact Dr. Michael Gill, Senior Lecturer in Psychiatry, Trinity Centre for Health Sciences, St. James' Hospital, James' St., Dublin 8, Ireland, Tel: 353-1-608-2241; FAX: 353-1-608-2241; e-mail: mgill@mail.tcd.ie

Molecular Psychiatry is an independent, peer-reviewed journal published by Stockton Press-Macmillan Press. Editorial decisions and publication in Molecular Psychiatry do not constitute endorsement by the National Institute of Mental Health, the National Institutes of Health or any branch of the government of the United States of America.

Editor: Julio Licinio, M.D.; phone: 301-496-6885; FAX: 301-402-1561; e-mail: licinio@nih.gov

Pre-prints of this article can be obtained from Ms. Julie Vianello; phone: 301-496-6979; FAX: 301-402-1561; e-mail: j.vianello@stockton-press.co.uk



Molecular Psychiatry

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