Please cite this article as follows: Li J, Kang C, Zhang H, Wang Y, Zhou R, Wang B, Guan L, Yang L, Faraone SV. 2007. Monoamine Oxidase A Gene Polymorphism Predicts Adolescent Outcome of Attention-Deficit/Hyperactivity Disorder. Am J Med Genet Part B 144B:430–433.
Article first published online: 10 APR 2007
Copyright © 2007 Wiley-Liss, Inc.
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume 144B, Issue 4, pages 430–433, 5 June 2007
How to Cite
Li, J., Kang, C., Zhang, H., Wang, Y., Zhou, R., Wang, B., Guan, L., Yang, L. and Faraone, S. V. (2007), Monoamine oxidase A gene polymorphism predicts adolescent outcome of attention-deficit/hyperactivity disorder. Am. J. Med. Genet., 144B: 430–433. doi: 10.1002/ajmg.b.30421
Jun Li and Chuanyuan Kang contributed equally to this work.
- Issue published online: 24 MAY 2007
- Article first published online: 10 APR 2007
- Manuscript Accepted: 18 JUL 2006
- Manuscript Received: 8 MAY 2006
- Ministry of Science and Technology, China. Grant Number: 2004BA720A20
- Project of Science and Technology, Beijing. Grant Number: Y0204003040831
- Key Project for Clinical Faculty Foundation, Ministry of Health, China. Grant Number: 2004-468
- attention-deficit/hyperactivity disorder (ADHD);
ADHD is generally deemed to be a highly heritable disorder with mean heritability of 0.75. The enzyme monoamine oxidase (MAO), which has both A and B types, has long been considered a candidate pathological substrate for ADHD, and more recently, the genes for both MAO enzymes have been examined as mediators of the illness. Previous studies indicated that 30–50% of children with ADHD will experience symptoms that persist into adolescence and will have more significant impairment in social and neuropsychological functioning compared to those whose symptoms have remitted. Genes may also influence these characteristics of the disorder, and in this context MAO genes may also be candidates for moderating the presentation of ADHD. The current study examined the association between adolescent outcome of ADHD and MAO gene polymorphisms, including the 941T > G polymorphism in exon 8 (rs1799835) and 1460C > T polymorphism in exon 14 (rs1137070) of the MAOA gene, and the A > G polymorphism in intron13 (rs1799836), C > T polymorphism in the 3'UTR (rs1040399), and 2327T > C polymorphism in exon15 of the MAOB gene. Significant associations were observed between the MAOA gene polymorphisms and ADHD remission. Due to the small sample size and the possibility of phenotypic and etiologic heterogeneity of ADHD outcomes across ethnic or geographic groups, these results must be replicated before they can be generalized to other populations. © 2007 Wiley-Liss, Inc.