No abstract

No abstract

Measures of component reading and language skills, executive functions, and processing speed were administered to groups of children with attention deficit hyperactivity disorder (ADHD; n = 113), reading disability (RD; n = 109), both RD and ADHD (n = 64), and neither RD nor ADHD (n = 151). Groups with RD exhibited pronounced deficits on all measures of component reading and language skills, as well as significant weaknesses on measures of verbal working memory, processing speed, and response inhibition. Groups with ADHD exhibited weaknesses on all response-inhibition and processing speed tasks and were impaired on some measures of component reading skills and verbal working memory. The group with comorbid RD and ADHD exhibited the combination of the deficits in the RD-only and ADHD-only groups, providing evidence against the phenocopy and cognitive subtype hypotheses as explanations for the co-occurrence of RD and ADHD. Slow and variable processing speed was characteristic of all 3 clinical groups, suggesting that measures of this domain may be useful for future studies that search for the common genes that increase susceptibility to RD and ADHD.

Conflict of interest statement: No conflicts declared.Freely available online through the PNAS open access option.

Although common sense suggests that environmental influences increasingly account for individual differences in behavior as experiences accumulate during the course of life, this hypothesis has not previously been tested, in part because of the large sample sizes needed for an adequately powered analysis. Here we show for general cognitive ability that, to the contrary, genetic influence increases with age. The heritability of general cognitive ability increases significantly and linearly from 41% in childhood (9 years) to 55% in adolescence (12 years) and to 66% in young adulthood (17 years) in a sample of 11 000 pairs of twins from four countries, a larger sample than all previous studies combined. In addition to its far-reaching implications for neuroscience and molecular genetics, this finding suggests new ways of thinking about the interface between nature and nurture during the school years. Why, despite life's 'slings and arrows of outrageous fortune', do genetically driven differences increasingly account for differences in general cognitive ability? We suggest that the answer lies with genotype-environment correlation: as children grow up, they increasingly select, modify and even create their own experiences in part based on their genetic propensities.

Several quantitative trait loci (QTLs) that influence developmental dyslexia (reading disability [RD]) have been mapped to chromosome regions by linkage analysis. The most consistently replicated area of linkage is on chromosome 6p23-21.3. We used association analysis in 223 siblings from the United Kingdom to identify an underlying QTL on 6p22.2. Our association study implicates a 77-kb region spanning the gene TTRAP and the first four exons of the neighboring uncharacterized gene KIAA0319. The region of association is also directly upstream of a third gene, THEM2. We found evidence of these associations in a second sample of siblings from the United Kingdom, as well as in an independent sample of twin-based sibships from Colorado. One main RD risk haplotype that has a frequency of approximately 12% was found in both the U.K. and U.S. samples. The haplotype is not distinguished by any protein-coding polymorphisms, and, therefore, the functional variation may relate to gene expression. The QTL influences a broad range of reading-related cognitive abilities but has no significant impact on general cognitive performance in these samples. In addition, the QTL effect may be largely limited to the severe range of reading disability.

This study used a nonreferred sample of twins to contrast the performance of individuals with reading disability (RD; n = 93), attention-deficit/hyperactivity disorder (ADHD; n = 52), RD and ADHD (n = 48), and neither RD nor ADHD (n = 121) on measures of phoneme awareness (PA) and executive functioning (EF). Exploratory factor analysis of the EF measures yielded underlying factors of working memory, inhibition, and set shifting. Results revealed that ADHD was associated with inhibition deficits, whereas RD was associated with significant deficits on measures of PA and verbal working memory. The RD + ADHD group was most impaired on virtually all measures, providing evidence against the phenocopy hypothesis as an explanation for comorbidity between RD and ADHD.

Phonological coding, measured by the oral reading of nonwords, and orthographic coding, measured by the discrimination of words from homophonic nonwords (e.g., rane, rain), were compared for pairs of older children with reading disabilities (RD) and younger nondisabled readers matched on word recognition. Phonological coding was substantially lower for most children with RD, indicating a unique developmental deficit in phonological coding rather than an equal developmental lag across all component reading skills. Data from identical and fraternal twins indicated that the phonological coding deficit of the children with RD was highly heritable and accounted for most of the heritable variance in their word recognition deficits. The deficits of the twins with RD in segmental language skills (rhyming and phoneme segmentation) were related to the heritable variance in their phonological coding deficits. Orthographic coding was not significantly heritable, and it accounted for much of the environmental variance in word recognition deficits. Implications of the results for the remediation of reading disability are discussed.