ArticleJournal of human genetics2017
The role of READ1 and KIAA0319 genetic variations in developmental dyslexia: testing main and interactive effects.
Article in Journal of human genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Targeted analysis of dyslexia-associated regions on chromosomes 6, 12 and 15 in large multigenerational cohorts.PloS one · 2025Article
- The Mediation Role of Dynamic Multisensory Processing Using Molecular Genetic Data in Dyslexia.Brain sciences · 2020Article
- Genetic association study of dyslexia and ADHD candidate genes in a Spanish cohort: Implications of comorbid samples.PloS one · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Developmental dyslexia (DD) is a complex heritable condition characterized by impaired reading abilities. Two well-replicated candidate risk factors are as follows: (1) regulatory element associated with dyslexia 1 (READ1), which is located in intron 2 of DCDC2 and acts as a binding site for protein regulation of DCDC2 expression; and (2) a three-single-nucleotide polymorphism risk haplotype spanning KIAA0319. Phylogenetically similar READ1 variants showed synergistic effects with the KIAA0319 risk haplotype on reading-related phenotypes in a general population sample. Here we examine the association between different allele classes in READ1, the KIAA0319 risk haplotype and reading-related traits in a cohort of 368 Italian children with DD and their siblings (n=266) by testing both main and non-additive effects. We replicated the deleterious main effects upon both reading accuracy and speed exerted by the longer READ1 alleles. We further supported the interdependence through non-additive, possibly antagonistic, effects between READ1 and the KIAA0319 risk haplotype on reading accuracy. By suggesting the presence of common biological processes underlying reading (dis)ability, these findings represent initial support for a generalist effect of the non-additive interdependence between READ1 and the KIAA0319 risk haplotype. Moreover, our results confirm that using as much information as possible about genetic interdependence among dyslexia-candidate genes can help in clinically assessing the individual risk for DD.
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