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Developmental dyslexia is a highly heritable disorder with a prevalence of at least 5% in school-aged children. Linkage studies have identified numerous loci throughout the genome that are likely to harbour candidate dyslexia susceptibility genes. Association studies and the refinement of chromosomal translocation break points in individuals with dyslexia have resulted in the discovery of candidate genes at some of these loci. A key function of many of these genes is their involvement in neuronal migration. This complements anatomical abnormalities discovered in dyslexic brains, such as ectopias, that may be the result of irregular neuronal migration.

AbstractBackgroundEarly intervention for children identified as late talkers (LTs) at the age of 24 months is still a controversial issue in research and clinical routine. Previous studies have shown inconsistent results regarding predictors of early lexical deficits on school‐age outcomes of late‐talking toddlers.MethodsIn a five‐wave follow‐up study, we investigated various aspects of language and literacy abilities in 39 German‐speaking third‐graders who had been identified as LTs at the age of 24 months, compared to 39 typically developing children (TDC) also attending the third grade. The duration of auditory sensory memory was examined at the age of 4 years using mismatch negativity (MMN) of tones – an event‐related potential not confounded by any language skill. In addition, the predictive value of memory performance was examined in a longitudinal perspective.ResultsOverall, LTs scored within normal range in language and literacy assessments. However, LTs differed from TDC in vocabulary size, verbalization of semantic relations, non‐word repetition, and spelling. The findings can be explained by phonological working memory. The duration of auditory sensory memory and spatial working memory did not account for any variance.ConclusionsLTs sustain persistent phonological processing limitations even though their native language and literacy performance lay within the normal range at school age. Further research on second language acquisition, academic achievements, and the efficacy of early intervention in late‐talking toddlers is recommended.

AbstractPeople with developmental dyslexia (DD) have been shown to be impaired in tasks that require the processing of multiple visual elements in parallel. It has been suggested that this deficit originates from disturbed visual attentional functions. The parameter‐based assessment of visual attention based on Bundesen's () theory of visual attention allows one to identify and quantify the underlying deficits. The present study provides the first groupwise comparison between children withDD(n = 12; mean age 9.84 years) and typically developing children (n = 12; mean age 9.87 years) with regard to intact and disturbed components of visual attention. From the performance on whole‐ and partial‐report tasks, we derived individual parameter estimates of four different parameters: visual processing speed, storage capacity of visual short‐term memory (VSTM), laterality of attentional weighting and efficiency of top‐down control. Groupwise comparisons revealed that general attentional resources, processing speed andVSTMstorage capacity, are impaired in children withDDcompared to typically developing children. In contrast, selectivity parameters, laterality of attentional selection and attentional top‐down control did not differ between these groups. Relating the current findings to previous results, obtained in highly comparable methodological settings, from single cases of children withDD, and from a group of adults withDD, we conclude that slowed perceptual processing speed is a primary visual attentional deficit inDD. Furthermore, reducedVSTMstorage capacity seems to modulate the difficulties in written language processing imposed by the disorder.

Funding: AG and TFMA were supported by the Munich Cluster for Systems Neurology (SyNergy). AG 535 was supported by Fondazione Umberto Veronesi. SP is a Royal Society University Research fellow. BMM, CF, BSP and SEF are supported by the Max Planck Society. AW, BM and HK were funded by the Fraunhofer Society and the Max Planck Society within the 'Pakt für Forschung und Innovation'. HK was also supported by LIFE – Leipzig Research Center for Civilization Diseases funded by means of the European Union; the European Regional Development Fund (ERDF); and the Free State of Saxony within the excellence initiative. FR is supported by Agence Nationale de la Recherche (ANR-06-NEURO-019-01, ANR-17-EURE-542 0017 IEC, ANR-10-IDEX-0001-02 PSL, ANR-11-BSV4-014-01), European Commission (LSHM-CT-2005-018696). TFMA was supported by the BMBF through the DIFUTURE consortium of the Medical Informatics Initiative Germany (grant 01ZZ1804A) and by the European Union's Horizon 2020 Research and Innovation Programme (grant MultipleMS, EU RIA 733161). ; 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 neuroimaging evidence. ; Publisher PDF ; Peer reviewed