Further evidence for the association between attention-deficit/hyperactivity disorder and the dopamine-β-hydroxylase gene

• Published in: American journal of medical genetics Vol. 114; no. 2; pp. 154 - 158
• Main Authors: Roman, Tatiana, Schmitz, Marcelo, Polanczyk, Guilherme V., Eizirik, Mariana, Rohde, Luis A., Hutz, Mara H.
• Format: Journal Article
• Language: English
• Published: New York Wiley Subscription Services, Inc., A Wiley Company 08-03-2002; Wiley-Liss
• Subjects: ADHD; Alleles; association; Attention Deficit Disorder with Hyperactivity - enzymology; Attention Deficit Disorder with Hyperactivity - genetics; Biological and medical sciences; DBH gene; Deoxyribonucleases, Type II Site-Specific - metabolism; DNA - genetics; DNA - metabolism; Dopamine beta-Hydroxylase - genetics; dopamine-β-hydroxylase; Family Health; Female; Gene Frequency; Genotype; Humans; Male; Medical genetics; Medical sciences; Mental and behavioral disorders; Nuclear Family; Polymorphism, Genetic; susceptibility; Human; Site; Impulsivity; Dopamine; Enzyme; Family study; Hyperactivity; Sample; Hydroxylase; Transmission; Risk analysis; Catecholamine; Symptomatology; Allele; Association; Gene; Dopamine agonist; Mental disorder; Norepinephrine; Oxidoreductases; Locus; Child; Haplotype; Polymorphism
• ISSN: 0148-7299; 1096-8628
• DOI: 10.1002/ajmg.10194

Attention‐deficit/hyperactivity disorder (ADHD) is a very common and heterogeneous psychiatric disorder of childhood with marked inattentive, hyperactive, and impulsive symptoms. The DBH gene, the locus that encodes the enzyme dopamine‐β‐hydroxylase (DβH), seems to be an important candidate gene for association studies, since DβH catalyzes the conversion of dopamine to norepinephrine. The aim of this study was to test for association between the DBH gene and ADHD in a sample of 88 Brazilian nuclear families. Haplotype relative risk (HRR) analysis of the DBH TaqI restriction site polymorphism showed a preferential transmission of the TaqI A2 allele in our whole ADHD sample (χ2 = 3.61, one‐tailed P = 0.03). The significant effect of the A2 allele was stronger when only families with no ADHD parental diagnosis were considered (χ2 = 5.42, one‐tailed P = 0.01). Our results suggest a contribution of this gene to ADHD susceptibility, partially replicating previous findings that have demonstrated an association between the DBH TaqI A2 allele and ADHD. © 2002 Wiley‐Liss, Inc.