Abstract
Independent studies have shown that candidate genes for dyslexia and specific language impairment (SLI) impact upon reading/language-specific traits in the general population. To further explore the effect of disorder-associated genes on cognitive functions, we investigated whether they play a role in broader cognitive traits. We tested a panel of dyslexia and SLI genetic risk factors for association with two measures of general cognitive abilities, or IQ, (verbal and non-verbal) in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (N>5,000). Only the MRPL19/C2ORF3 locus showed statistically significant association (minimum P = 0.00009) which was further supported by independent replications following analysis in four other cohorts. In addition, a fifth independent sample showed association between the MRPL19/C2ORF3 locus and white matter structure in the posterior part of the corpus callosum and cingulum, connecting large parts of the cortex in the parietal, occipital and temporal lobes. These findings suggest that this locus, originally identified as being associated with dyslexia, is likely to harbour genetic variants associated with general cognitive abilities by influencing white matter structure in localised neuronal regions.
Highlights
Dyslexia and specific language impairment (SLI) are common neurodevelopmental disorders, reflecting specific deficits in the acquisition of literacy skills and oral language, respectively [1]
Given the high correlation between verbal IQ (VIQ) and READ (r = 0.571; Table 1) [11], it is plausible that the association we observed here was driven by reading ability
We evaluated the effect of candidate genes for RD and SLI on measures of general cognitive ability in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort
Summary
Dyslexia (or reading disability, RD) and specific language impairment (SLI) are common neurodevelopmental disorders, reflecting specific deficits in the acquisition of literacy skills and oral language, respectively [1]. For both disorders, a diagnosis is achieved by excluding known causes of the deficits, such as cooccurring sensory or neurological impairment or lack of educational opportunity. It has been shown that most of the dyslexia risk genes (KIAA0319, DCDC2, DYX1C1 and ROBO1) are involved in cortical development and in neuronal migration [4]. An important unanswered research question is how genes involved in such a general process as cortical development contribute to the risk for specific neurodevelopmental disorders.
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