A neural index of inefficient evidence accumulation in dyslexia underlying slow perceptual decision making.

Visual processing deficits have been widely reported in developmental dyslexia however the locus of cognitive dysfunction remains unclear. Here, we examined the neural correlates of perceptual decision-making using a dot-motion task and electroencephalography (EEG) and investigated whether presenting deficits were unique to children with dyslexia or if they were also evident in other, typically developing children with equally immature reading systems. Sixty-eight children participated: 32 with dyslexia (DD; 16 females); 21 age-matched controls (AM; 11 females) and 15 reading-matched controls (RM; 9 females). All participants completed a bilaterally presented random-dot-motion task while EEG was recorded. Neural signatures of low level sensory processing (steady state visual evoked potentials; SSVEPs), pre-target attentional bias (posterior α power), attentional orienting (N2), evidence accumulation (centro-parietal positive decision signal; CPP) and execution of a motor response (ß) were obtained to dissect the temporal sequence of perceptual decision-making. Reading profile provided a score of relative lexical and sublexical skills for each participant. Although all groups performed comparably in terms of task accuracy and false alarm rate, the DD group were slower and demonstrated an earlier peak latency, reduced slope and lower amplitude of the CPP compared with both AM and RM controls. Reading profile was found to moderate the relationship between word reading ability, reaction time as well as CPP indices showing that lexical dyslexics responded more slowly and had a shallower slope, reduced amplitude and earlier latency of CPP waveforms than sublexical dyslexics. These findings suggest that children with dyslexia, particularly those with relatively poorer lexical abilities, have a reduced rate and peak of evidence accumulation as denoted by CPP markers yet remain slow in their overt response. This is in keeping with hypotheses that children with dyslexia have impairment in effectively sampling and processing evidence about visual motion stimuli.

An association between a dopamine transporter gene (SLC6A3) haplotype and ADHD symptom measures in nonclinical adults.

Previous genetic studies have postulated that attention deficit hyperactivity disorder (ADHD) should be regarded as the extreme end of a set of behavioural traits that can be continuously measured in the general population. The current study adopted a quantitative trait approach to examine the relationship between dopamine gene variants and self-reported ADHD symptoms in 517 nonclinical adults. Although genetic associations with variants of both the dopamine transporter (DAT1; SLC6A3) and D4 receptor (DRD4) genes have been reliably reported in children, results in adults are less consistent. We probed two potentially functional variable number of tandem repeat (VNTR) polymorphisms in the 3'UTR and intron 8 of DAT1, the 10-repeat and 6-repeat alleles of which respectively form a haplotype (10/6 DAT1 haplotype) that is associated with childhood ADHD. We also genotyped the exon 3 VNTR of DRD4, the 7-repeat allele of which is also an established risk factor for childhood ADHD. Permutation analysis showed an influence of the 10/6 DAT1 haplotype on both CAARS-G and CAARS-H (DSM-IV ADHD Symptoms Total and ADHD Index respectively), such that ADHD symptom scores increased with each additional copy of the 10/6 DAT1 haplotype. This result survived corrections for multiple comparisons both at the level of genotype and phenotype. A nominal association with CAARS-G was also found for the 7-repeat allele of the DRD4 VNTR however this did not survive multiple comparison correction. Our results provide further support for the influence of variation in the 10/6 DAT1 haplotype and individual differences in ADHD symptoms in adults.