ArticleMolecular psychiatry2011
First genome-wide association scan on neurophysiological endophenotypes points to trans-regulation effects on SLC2A3 in dyslexic children.
Article in Molecular psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- A systematic review and meta-analysis of imaging genetics studies of specific reading disorder.Cognitive neuropsychology · 2021Pooled it
- Neuroprotection by canagliflozin in a Huntington's disease model: role of HIF-1α and PI3K/AKT signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Natural selection and language genes in humans.Scientific reports · 2026Article
- Neurodevelopment Is Dependent on Maternal Diet: Placenta and Brain Glucose Transporters GLUT1 and GLUT3.Nutrients · 2024Review
- Brain structure, phenotypic and genetic correlates of reading performance.Nature human behaviour · 2023Article
- Genome-wide association study reveals new insights into the heritability and genetic correlates of developmental dyslexia.Molecular psychiatry · 2021Article
- The Polygenic Nature and Complex Genetic Architecture of Specific Learning Disorder.Brain sciences · 2021Review
- Adult glut3 homozygous null mice survive to demonstrate neural excitability and altered neurobehavioral responses reminiscent of neurodevelopmental disorders.Experimental neurology · 2021Article
- Neuroimaging genetics studies of specific reading disability and developmental language disorder: A review.Language and linguistics compass · 2019Article
- Genome-wide association scan identifies new variants associated with a cognitive predictor of dyslexia.Translational psychiatry · 2019Article
- White matter network connectivity deficits in developmental dyslexia.Human brain mapping · 2019Article
- Transcript Analysis of Zebrafish GLUT3 Genes,Frontiers in molecular neuroscience · 2019Article
- Neural Deletion of Glucose Transporter Isoform 3 Creates Distinct Postnatal and Adult Neurobehavioral Phenotypes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Effective Instruction for Persisting Dyslexia in Upper Grades: Adding Hope Stories and Computer Coding to Explicit Literacy Instruction.Education and information technologies · 2018Article
- Ancestral Variations of the PCDHG Gene Cluster Predispose to Dyslexia in a Multiplex Family.EBioMedicine · 2018Article
- Genetic association study of dyslexia and ADHD candidate genes in a Spanish cohort: Implications of comorbid samples.PloS one · 2018Article
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- Neurobiological bases of reading disorder Part I: Etiological investigations.Language and linguistics compass · 2017Article
- Neurogenetics of developmental dyslexia: from genes to behavior through brain neuroimaging and cognitive and sensorial mechanisms.Translational psychiatry · 2017Review
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dyslexia is one of the most common learning disorders affecting about 5% of all school-aged children. It has been shown that event-related potential measurements reveal differences between dyslexic children and age-matched controls. This holds particularly true for mismatch negativity (MMN), which reflects automatic speech deviance processing and is altered in dyslexic children. We performed a whole-genome association analysis in 200 dyslexic children, focusing on MMN measurements. We identified rs4234898, a marker located on chromosome 4q32.1, to be significantly associated with the late MMN component. This association could be replicated in an independent second sample of 186 dyslexic children, reaching genome-wide significance in the combined sample (P = 5.14e-08). We also found an association between the late MMN component and a two-marker haplotype of rs4234898 and rs11100040, one of its neighboring single nucleotide polymorphisms (SNPs). In the combined sample, this marker combination withstands correction for multiple testing (P = 6.71e-08). Both SNPs lie in a region devoid of any protein-coding genes; however, they both show significant association with mRNA-expression levels of SLC2A3 on chromosome 12, the predominant facilitative glucose transporter in neurons. Our results suggest a possible trans-regulation effect on SLC2A3, which might lead to glucose deficits in dyslexic children and could explain their attenuated MMN in passive listening tasks.
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