Monash University, School of Psychology and Psychiatry, Victoria, Australia.
Trinity College Dublin, School of Psychology and Trinity College Institute of Neuroscience, Dublin, Ireland.
Neuropsychologia. 2012 Oct;50(12):2823-2829. doi: 10.1016/j.neuropsychologia.2012.08.012. Epub 2012 Aug 23.
A number of recent studies suggest that DNA variation in the dopamine transporter gene (DAT1) influences spatial attention asymmetry in clinical populations such as ADHD, but confirmation in non-clinical samples is required. Since non-spatial factors such as attentional load have been shown to influence spatial biases in clinical conditions, here we sought to determine whether any association between DAT1 genotype and spatial bias might be moderated by non-spatial attentional load. Healthy adults were asked to react to sudden onset peripheral targets while demand on non-spatial attention was manipulated via a central task. Participants were genotyped for a DAT1 variable number of tandem repeat (VNTR) polymorphism. The 10-repeat allele of this variant is a replicated susceptibility allele for ADHD and has been shown to associate with spatial bias. As expected, an overall leftward asymmetry/pseudoneglect was observed when the data were averaged across the entire sample. When data were stratified by DAT1 genotype, individuals lacking homozygosity for the 10-repeat DAT1 allele (non-10/10) showed a pronounced leftward bias that was significantly different from zero. In line with past reports from children with ADHD, this leftward bias was attenuated in individuals who were homozygous for the DAT1 10-repeat allele (10/10), suggestive of relatively weaker right hemisphere dominance for spatial attention. This effect of DAT1 genotype on spatial bias was not modulated by non-spatial attention load. These data confirm in healthy adult participants both the existence and the direction of the relationship previously reported between DAT1 genotype and spatial bias in children with ADHD. These data add to a growing body of evidence showing that spatial attentional asymmetry is a stable quantitative trait, with individual differences in this trait significantly predicted by common DNA variation in the DAT1 gene.
一些最近的研究表明，多巴胺转运蛋白基因（DAT1）中的 DNA 变异会影响 ADHD 等临床人群的空间注意力不对称，但需要在非临床样本中得到证实。由于注意力负荷等非空间因素已被证明会影响临床条件下的空间偏向，因此我们在这里试图确定 DAT1 基因型与空间偏向之间的任何关联是否可能受到非空间注意力负荷的调节。健康成年人被要求对外周突发目标做出反应，同时通过中央任务来操纵非空间注意力的需求。参与者的 DAT1 可变数串联重复（VNTR）多态性进行了基因分型。该变体的 10 个重复等位基因是 ADHD 的复制易感性等位基因，并且与空间偏向有关。正如预期的那样，当将整个样本的数据平均化时，观察到总体上的左偏/假性忽视。当根据 DAT1 基因型对数据进行分层时，缺乏 10 重复 DAT1 等位基因（非 10/10）纯合性的个体表现出明显的左偏，与零显著不同。与 ADHD 儿童的过去报告一致，10 重复 DAT1 等位基因（10/10）纯合的个体中这种左偏被减弱，提示空间注意力的右半球优势相对较弱。DAT1 基因型对空间偏向的这种影响不受非空间注意力负荷的调节。这些数据在健康成年参与者中证实了先前在 ADHD 儿童中报告的 DAT1 基因型与空间偏向之间的存在和关系的方向。这些数据增加了越来越多的证据，表明空间注意力不对称是一种稳定的定量特征，个体在这种特征上的差异可由 DAT1 基因中的常见 DNA 变异显著预测。
