Candidate gene studies of ADHD: a meta-analytic review

被引:739
作者
Gizer, Ian R. [1 ]
Ficks, Courtney [2 ]
Waldman, Irwin D. [2 ]
机构
[1] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA
[2] Emory Univ, Dept Psychol, Atlanta, GA 30322 USA
基金
美国国家卫生研究院;
关键词
ATTENTION-DEFICIT-HYPERACTIVITY; DOPAMINE TRANSPORTER GENE; CATECHOL-O-METHYLTRANSFERASE; FAMILY-BASED ASSOCIATION; MONOAMINE-OXIDASE-A; ALPHA-2A ADRENERGIC-RECEPTOR; TANDEM DUPLICATION POLYMORPHISM; ACETYLCHOLINE-RECEPTOR-ALPHA-4 SUBUNIT GENE; DEFICIT/HYPERACTIVITY DISORDER ADHD; ACTIVITY-DEPENDENT SECRETION;
D O I
10.1007/s00439-009-0694-x
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Quantitative genetic studies (i.e., twin and adoption studies) suggest that genetic influences contribute substantially to the development of attention deficit hyperactivity disorder (ADHD). Over the past 15 years, considerable efforts have been made to identify genes involved in the etiology of this disorder resulting in a large and often conflicting literature of candidate gene associations for ADHD. The Wrst aim of the present study was to conduct a comprehensive meta-analytic review of this literature to determine which candidate genes show consistent evidence of association with childhood ADHD across studies. The second aim was to test for heterogeneity across studies in the effect sizes for each candidate gene as its presence might suggest moderating variables that could explain inconsistent results. Significant associations were identified for several candidate genes including DAT1, DRD4, DRD5, 5HTT, HTR1B, and SNAP25. Further, significant heterogeneity was observed for the associations between ADHD and DAT1, DRD4, DRD5, DBH, ADRA2A, 5HTT, TPH2, MAOA, and SNAP25, suggesting that future studies should explore potential moderators of these associations (e.g., ADHD subtype diagnoses, gender, exposure to environmental risk factors). We conclude with a discussion of these findings in relation to emerging themes relevant to future studies of the genetics of ADHD.
引用
收藏
页码:51 / 90
页数:40
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