Linkage studies between attention-deficit hyperactivity disorder and the monoamine oxidase genes

Citation
Sd. Jiang et al., Linkage studies between attention-deficit hyperactivity disorder and the monoamine oxidase genes, AM J MED G, 105(8), 2001, pp. 783-788
Citations number
28
Categorie Soggetti
Molecular Biology & Genetics
Journal title
AMERICAN JOURNAL OF MEDICAL GENETICS
ISSN journal
01487299 → ACNP
Volume
105
Issue
8
Year of publication
2001
Pages
783 - 788
Database
ISI
SICI code
0148-7299(200112)105:8<783:LSBAHD>2.0.ZU;2-V
Abstract
Attention-deficit hyperactivity disorder (ADHD) is a prevalent behavioral d isorder in children and the etiology of this disorder is not clear. Molecul ar genetic and pharmacological studies suggest the involvement of dopaminer gic and noradrenergic neurotransmitter systems in ADHD, e.g., several repor ts have found association between ADHD and the dopamine receptor gene DRD-4 , the dopamine transporter gene DAT1, and the catecholamine clearance enzym e catechol-O-methyltransferase. Monoamine oxidase (MAO) A and B genes encod e enzymes that participate in the metabolism of neurotransmitters of the do paminergic and noradrenergic systems. MAO inhibitors have been shown to be effective in the treatment of ADHD. Our previous studies showed an associat ion between ADHD and the DXS7 locus, which is located in close vicinity to the MAO genes on chromosome X. These findings suggest that there might be l inkage between ADHD and MAO genes. To test this hypothesis, we used the tra nsmission/disequilibrium test (TDT) to test for linkage between a VNTR poly morphism at the MAOA(CA)(n) or MAOB(GT)(n) locus and DSM-III-R-diagnosed AD HD in 82 nuclear families of the Chinese population. The TDT analysis revea led linkage between ADHD and the MAOA(CA)n locus (chi-square = 15.25, df = 7, P < 0.05), but not the MAOB(GT). locus (chi-square = 11.18, df = 7, P > 0.05). The data showed that ADHD was in linkage with the MAOA gene and sugg ested that MAOA might be a susceptibility factor for ADHD. (C) 2001 Wiley-L iss, Inc.