ArticleTranslational psychiatry2017
The DCDC2 deletion is not a risk factor for dyslexia.
Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.
What it found
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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.
The trial behind it
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Who cites it
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.
- Hypothesis-driven genome-wide association studies provide novel insights into genetics of reading disabilities.Translational psychiatry · 2022Pooled it
- Language and reading impairments are associated with increased prevalence of non-right-handedness.Child developmentPooled it
- Associations between READ1 deletion, reading proficiency, and white matter network organisation in children with and without developmental dyslexia.Brain structure & function · 2026Article
- Whole-exome sequencing in children with dyslexia implicates rare variants in CLDN3 and ion channel genes.Human genetics · 2025Article
- Alterations in neural activation in the ventral frontoparietal network during complex magnocellular stimuli in developmental dyslexia associated with READ1 deletion.Behavioral and brain functions : BBF · 2024Article
- Article
- Animal models of developmental dyslexia.Frontiers in neuroscience · 2022Review
- White matter deficits correlate with visual motion perception impairments in dyslexic carriers of the DCDC2 genetic risk variant.Experimental brain research · 2021Article
- A rare missense variant in the ATP2C2 gene is associated with language impairment and related measures.Human molecular genetics · 2021Article
- Effect of READ1 on latent profiles of reading disorder and comorbid attention and language impairment subtypes.Child neuropsychology : a journal on normal and abnormal development in childhood and adolescence · 2020Article
- Neuroimaging genetics studies of specific reading disability and developmental language disorder: A review.Language and linguistics compass · 2019Article
- What Factors Facilitate Resilience in Developmental Dyslexia? Examining Protective and Compensatory Mechanisms Across the Neurodevelopmental Trajectory.Child development perspectives · 2018Article
- The neuronal migration hypothesis of dyslexia: A critical evaluation 30 years on.The European journal of neuroscience · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 8 institutions in 3 countries.
Funding
Abstract
Dyslexia is a specific impairment in learning to read and has strong heritability. An intronic deletion within the DCDC2 gene, with ~8% frequency in European populations, is increasingly used as a marker for dyslexia in neuroimaging and behavioral studies. At a mechanistic level, this deletion has been proposed to influence sensory processing capacity, and in particular sensitivity to visual coherent motion. Our re-assessment of the literature, however, did not reveal strong support for a role of this specific deletion in dyslexia. We also analyzed data from five distinct cohorts, enriched for individuals with dyslexia, and did not identify any signal indicative of associations for the DCDC2 deletion with reading-related measures, including in a combined sample analysis (N=526). We believe we conducted the first replication analysis for a proposed deletion effect on visual motion perception and found no association (N=445 siblings). We also report that the DCDC2 deletion has a frequency of 37.6% in a cohort representative of the general population recruited in Hong Kong (N=220). This figure, together with a lack of association between the deletion and reading abilities in this cohort, indicates the low likelihood of a direct deletion effect on reading skills. Therefore, on the basis of multiple strands of evidence, we conclude that the DCDC2 deletion is not a strong risk factor for dyslexia. Our analyses and literature re-evaluation are important for interpreting current developments within multidisciplinary studies of dyslexia and, more generally, contribute to current discussions about the importance of reproducibility in science.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.