Relations Between Multi-Informant Assessments of ADHD Symptoms, DAT1, and DRD4
Relations Between Multi-Informant Assessments of ADHD Symptoms, DAT1, and DRD4
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DOI：
10.1037/a0013297
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发表时间：
2008-11-01
影响因子：
4.6
通讯作者：
Rowe, David C.
中科院分区：
文献类型：
--
作者：
Gizer, Ian R.;Waldman, Irwin D.;Rowe, David C.
进行注意力缺陷/多动障碍（ADHD）候选基因研究的研究人员通常从多个信息提供者那里获得症状评级（即，母亲、父亲和教师），并使用心理学家的最佳估计或简单的算法，例如在被调查者中获得最高的症状评分，以构建诊断表型来估计关联。尽管如此，这些方法从未在分子遗传学研究的背景下得到经验验证。在目前的研究中，作者系统地评估了几种操作表型的方法以及ADHD与候选基因之间的关联证据：多巴胺转运蛋白基因（DAT 1）和多巴胺D4受体基因（DRD 4）。在回归分析中使用症状评分作为连续量表表明，母亲和教师评分的组合产生了最强有力的证据，多动-冲动型ADHD症状和DAT 1之间的关联，以及注意力不集中的ADHD症状和DRD 4之间的关联。教师评分本身就足以评估注意力不集中症状和DAT 1之间的关联。此外，这种基于回归的方法始终比三种简单算法（即，和、或和平均规则）。这些结果对未来ADHD的分子遗传学研究的影响进行了讨论。
Researchers conducting candidate gene studies of attention-deficit/hyperactivity disorder (ADHD) typically obtain symptom ratings from multiple informants (i.e., mothers, fathers, and teachers) and use a psychologist's best estimate or a simple algorithm, such as taking the highest symptom ratings across informants, to construct diagnostic phenotypes for estimating association. Nonetheless, these methods have never been empirically validated in the context of a molecular genetic study. In the current study, the authors systematically evaluated several methods of operationalizing phenotypes and the resulting evidence for association between ADHD and the candidate genes: dopamine transporter gene (DAT1) and dopamine D4 receptor gene (DRD4). Use of symptom scores as continuous scales in regression analysis suggested that the combination of mother and teacher ratings yielded the strongest evidence for association between hyperactive-impulsive ADHD symptoms and DAT1 and between inattentive ADHD symptoms and DRD4. Teacher ratings alone were sufficient for evaluating the association between inattentive symptoms and DAT1. Further, this regression-based method consistently yielded stronger evidence for association among ADHD symptoms, DAT1, and DRD4 than did three simple algorithms (i.e., the and, or, and averaging rules). The implications of these results for future molecular genetic studies of ADHD are discussed.