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The use of spoken and written language is a fundamental human capacity. Individual differences in reading- and language-related skills are influenced by genetic variation, with twin-based heritability estimates of 30-80%, depending on the trait. The genetic architecture is complex, heterogeneous, and multifactorial, but investigations of contributions of single-nucleotide polymorphisms (SNPs) were thus far underpowered. We present a multicohort genome-wide association study (GWAS) of five traits assessed individually using psychometric measures: word reading, nonword reading, spelling, phoneme awareness, and nonword repetition, in samples of 13,633 to 33,959 participants aged 5-26 years. We identified genome-wide significant association with word reading (rs11208009, p=1.098 x 10-8) at a locus that has not been associated with intelligence or educational attainment. All five reading-/language-related traits showed robust SNP-heritability, accounting for 13-26% of trait variability. Genomic structural equation modelling revealed a shared genetic factor explaining most variation in word/nonword reading, spelling, and phoneme awareness, which only partially overlapped with genetic variation contributing to nonword repetition, intelligence and educational attainment. A multivariate GWAS of word/nonword reading, spelling, and phoneme awareness maximized power for follow-up investigation. Genetic correlation analysis of multivariate GWAS results with neuroimaging traits identified association with the surface area of the banks of the left superior temporal sulcus, a brain region linked to processing of spoken and written language. Heritability was enriched for genomic elements regulating gene expression in the fetal brain, and in chromosomal regions that are depleted of Neanderthal variants. Together, these results provide new avenues for deciphering the biological underpinnings of uniquely human traits.

While children are able to name letters fairly quickly, the automatisation of letter-speech sound mappings continues over the first years of reading development. In the current longitudinal fMRI study, we explored developmental changes in cortical responses to letters and speech sounds across 3 yearly measurements in a sample of 18 8–11 year old children. We employed a text-based recalibration paradigm in which combined exposure to text and ambiguous speech sounds shifts participants’ later perception of the ambiguous sounds towards the text. Our results showed that activity of the left superior temporal and lateral inferior precentral gyri followed a non-linear developmental pattern across the measurement sessions. This pattern is reminiscent of previously reported inverted-u-shape developmental trajectories in children’s visual cortical responses to text. Our findings suggest that the processing of letters and speech sounds involves non-linear changes in the brain’s spoken language network possibly related to progressive automatisation of reading skills.

This chapter assesses the acquisition of academic knowledge and skills in domains including literacy, numeracy, sciences, arts and physical education. It examines how learning trajectories arise from complex interactions between individual brain development and sociocultural environments. Teaching literacy and numeracy to all students is a goal of most school systems. While there are some fundamental skills children should grasp to succeed in these domains, the best way to support each student’s learning varies depending on their individual development, language, culture and prior knowledge. Here we explore considerations for instruction and assessment in diferent academic domains. To accommodate the fourishing of all children, fexibility must be built into education systems, which need to acknowledge the diverse ways in which children can progress through learning trajectories and demonstrate their knowledge.

The different ways students deal with mistakes is an integral part of mindset theory. While previous error-monitoring studies found supporting neural evidence for mindset-related differences, they may have been confounded by overlapping stimulus processing. We therefore investigated the relationship between mindset and event-related potentials (ERPs) of error-monitoring (response-locked Ne, Pe), with and without overlap correction. In addition, besides behavioral measures of remedial action after errors (post-error slowing and accuracy), we investigated their neural correlates (stimulus-locked N2). Results indicated comparable Ne, but larger Pe amplitudes in fixed-minded students; however, after overlap correction, the Pe results were rendered non-significant. A likely explanation for this overlap was a near-significant effect of mindset on the preceding stimulus P3. Finally, although N2 was larger for trials following errors, mindset was unrelated. The current study shows that the relationship between error-monitoring and mindset is more complex and should be reconsidered. Future studies are advised to explore stimulus processing as well, and if needed, to correct for stimulus overlap. In addition, contextual influences on and individual variation in error-monitoring need more scrutiny, which may contribute to refining mindset theory.

Reading acquisition reorganizes existing brain networks for speech and visual processing to form novel audio-visual language representations. This requires substantial cortical plasticity that is reflected in changes in brain activation and functional as well as structural connectivity between brain areas. The extent to which a child’s brain can accommodate these changes may underlie the high variability in reading outcome in both typical and dyslexic readers. In this review, we focus on reading-induced functional changes of the dorsal speech network in particular and discuss how its reciprocal interactions with the ventral reading network contributes to reading outcome. We discuss how the dynamic and intertwined development of both reading networks may be best captured by approaching reading from a skill learning perspective, using audio-visual learning paradigms and longitudinal designs to follow neuro-behavioral changes while children’s reading skills unfold.

One of the proposed issues underlying reading difficulties in dyslexia is insufficiently automatized letter-speech sound associations. In the current fMRI experiment, we employ text-based recalibration to investigate letter- speech sound mappings in 8–10 year-old children with and without dyslexia. Here an ambiguous speech sound /a?a/ midway between /aba/ and /ada/ is combined with disambiguating “aba” or “ada” text causing a perceptual shift of the ambiguous /a?a/ sound towards the text (recalibration). This perceptual shift has been found to be reduced in adults but not in children with dyslexia compared to typical readers. Our fMRI results show significantly reduced activation in the left fusiform in dyslexic compared to typical readers, despite comparable behavioural performance. Furthermore, enhanced audio-visual activation within this region was linked to better reading and phonological skills. In contrast, higher activation in bilateral superior temporal cortex was associated with lower letter-speech sound identification fluency. These findings reflect individual differences during the early stages of reading development with reduced recruitment of the left fusiform in dyslexic readers together with an increased involvement of the superior temporal cortex in children with less automatized letter-speech sound associations.

Developmental dyslexia (DD) is a learning disorder affecting the ability to read, with a heritability of 40-60%. A notable part of this heritability remains unexplained, and large genetic studies are warranted to identify new susceptibility genes and clarify the genetic bases of dyslexia. We carried out a genome-wide association study (GWAS) on 2274 dyslexia cases and 6272 controls, testing associations at the single variant, gene, and pathway level, and estimating heritability using single-nucleotide polymorphism (SNP) data. We also calculated polygenic scores (PGSs) based on large-scale GWAS data for different neuropsychiatric disorders and cortical brain measures, educational attainment, and fluid intelligence, testing them for association with dyslexia status in our sample. We observed statistically significant (p < 2.8 × 10$^{-6}$) enrichment of associations at the gene level, for LOC388780 (20p13; uncharacterized gene), and for VEPH1 (3q25), a gene implicated in brain development. We estimated an SNP-based heritability of 20-25% for DD, and observed significant associations of dyslexia risk with PGSs for attention deficit hyperactivity disorder (at p$_{T}$ = 0.05 in the training GWAS: OR = 1.23[1.16; 1.30] per standard deviation increase; p = 8 × 10$^{-13}$), bipolar disorder (1.53[1.44; 1.63]; p = 1 × 10$^{-43}$), schizophrenia (1.36[1.28; 1.45]; p = 4 × 10$^{-22}$), psychiatric cross-disorder susceptibility (1.23[1.16; 1.30]; p = 3 × 10$^{-12}$), cortical thickness of the transverse temporal gyrus (0.90[0.86; 0.96]; p = 5 × 10$^{-4}$), educational attainment (0.86[0.82; 0.91]; p = 2 × 10$^{-7}$), and intelligence (0.72[0.68; 0.76]; p = 9 × 10$^{-29}$). This study suggests an important contribution of common genetic variants to dyslexia risk, and novel genomic overlaps with psychiatric conditions like bipolar disorder, schizophrenia, and cross-disorder susceptibility. Moreover, it revealed the presence of shared genetic foundations with a neural correlate p

Developmental dyslexia (DD) is a learning disorder affecting the ability to read, with a heritability of 40–60%. A notable part of this heritability remains unexplained, and large genetic studies are warranted to identify new susceptibility genes and clarify the genetic bases of dyslexia. We carried out a genome-wide association study (GWAS) on 2274 dyslexia cases and 6272 controls, testing associations at the single variant, gene, and pathway level, and estimating heritability using single-nucleotide polymorphism (SNP) data. We also calculated polygenic scores (PGSs) based on large-scale GWAS data for different neuropsychiatric disorders and cortical brain measures, educational attainment, and fluid intelligence, testing them for association with dyslexia status in our sample. We observed statistically significant (p < 2.8 × 10−6) enrichment of associations at the gene level, for LOC388780 (20p13; uncharacterized gene), and for VEPH1 (3q25), a gene implicated in brain development. We estimated an SNP-based heritability of 20–25% for DD, and observed significant associations of dyslexia risk with PGSs for attention deficit hyperactivity disorder (at pT = 0.05 in the training GWAS: OR = 1.23[1.16; 1.30] per standard deviation increase; p = 8 × 10−13), bipolar disorder (1.53[1.44; 1.63]; p = 1 × 10−43), schizophrenia (1.36[1.28; 1.45]; p = 4 × 10−22), psychiatric cross-disorder susceptibility (1.23[1.16; 1.30]; p = 3 × 10−12), cortical thickness of the transverse temporal gyrus (0.90[0.86; 0.96]; p = 5 × 10−4), educational attainment (0.86[0.82; 0.91]; p = 2 × 10−7), and intelligence (0.72[0.68; 0.76]; p = 9 × 10−29). This study suggests an important contribution of common genetic variants to dyslexia risk, and novel genomic overlaps with psychiatric conditions like bipolar disorder, schizophrenia, and cross-disorder susceptibility. Moreover, it revealed the presence of shared genetic foundations with a neural correlate previously implicated in dyslexia by neuroimagin