Article

Noradrenergic genotype predicts lapses in sustained attention

Trinity College Institute of Neuroscience, Trinity College Dublin, Ireland.
Neuropsychologia (Impact Factor: 3.45). 11/2008; 47(2):591-4. DOI: 10.1016/j.neuropsychologia.2008.10.003
Source: PubMed

ABSTRACT Sustained attention is modulated by the neurotransmitter noradrenaline. The balance of dopamine and noradrenaline in the cortex is controlled by the DBH gene. The principal variant in this gene is a C/T change at position -1021, and the T allele at this locus is hypothesised to result in a slower rate of dopamine to noradrenaline conversion than the C allele. Two hundred participants who were genotyped for the DBH C-1021T marker performed the Sustained Attention to Response Task (SART). DBH genotype was found to significantly predict performance; participants with more copies of the T allele made more errors of commission, indicative of lapses in sustained attention. A significant negative correlation was also observed for all participants between errors of commission and mean reaction time. The decrease in noradrenaline occasioned by the T allele may impair sustained attention by reducing participants' ability to remain alert throughout the task and by increasing their susceptibility to distractors.

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Available from: Ciara M Greene, Jun 24, 2015
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    • "Because there is a strong influence of NE on sustained attention, genetic variants of noradrenergic genes may be associated with sustained attention phenotypes. Three studies have described associations between polymorphisms of DBH and sustained attention (Bellgrove et al., 2006; Greene et al., 2009; Kieling, Genro, Hutz, & Rohde, 2008). Another study that investigated ADRA2A revealed an association with response time variability of CPT (Cho et al., 2008), a finding that was later replicated to some extent (Kim et al., 2013). "
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    ABSTRACT: To investigate the genetic contributors to ADHD sustained attention deficit among noradrenergic genes responsible for the synthesis (dopamine-β-hydroxylase gene, DBH), transport (norepinephrine transporter gene, NET1), reception (alpha-2A adrenergic receptor gene, ADRA2A), and metabolism (monoamine oxidase A gene, MAOA) of noradrenalin (NE). A total of 456 children with ADHD and 108 normal controls were included in a digit cancellation test (DCT). DNA was collected from 242 participants and genotyped for 14 single nucleotide polymorphisms (SNPs) of noradrenergic genes. Compared with normal controls, children with ADHD showed a lower total score and higher mean error rate in the DCT, indicating poorer sustained attention function. Analysis of covariance showed an association between MAOA genotypes and ADHD performance in DCT, with poorer performance in risk allele carriers. No association was found for other noradrenergic genes. Children with ADHD presented with a sustained attention deficit compared with normal controls. The sustained attention deficit of children with ADHD may be associated with genetic variant of MAOA. © 2015 SAGE Publications.
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