SNP Sets and Reading Ability: Testing Confirmation of a 10-SNP Set in a Population Sample

Luciano, Michelle; Montgomery, Grant W.; Martin, Nicholas G.; Wright, Margaret J.; Bates, Timothy C.

doi:10.1375/twin.14.3.228

Cited by 6 publications

(10 citation statements)

References 28 publications

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“…Our families also generated a linkage signal at 9q31.2 (lod 1.52, 109.9 Mb, Table 1), which is close to a previous report of linkage to spelling ability at 9q31.3 (lod 1.2, D9S1677, 111.0 Mb, Loo et al 2004). Our localization is also supported by results of the first high density QTL association genome screen for early reading ability (Meaburn et al 2008), which found and replicated an association with rs1323381 at 110.10 Mb (although this association was not replicated by Luciano et al 2011). A possible regional candidate is AL390170 at 110.93 Mb, an uncharacterized clone highly expressed in fetal and adult brain.…”

Section: Other Regions (Lod 15-23)supporting

confidence: 75%

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Dense‐map genome scan for dyslexia supports loci at 4q13, 16p12, 17q22; suggests novel locus at 7q36

Field

Shumansky

Ryan

et al. 2012

Genes Brain and Behavior

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Analysis of genetic linkage to dyslexia was performed using 133,165 array-based SNPs genotyped in 718 persons from 101 dyslexia-affected families. Results showed five linkage peaks with lod scores >2.3 (4q13.1, 7q36.1-q36.2, 7q36.3, 16p12.1, and 17q22). Of these five regions, three have been previously implicated in dyslexia (4q13.1, 16p12.1, and 17q22), three have been implicated in attention-deficit hyperactivity disorder (ADHD, which highly co-occurs with dyslexia; 4q13.1, 7q36.3, 16p12.1) and four have been implicated in autism (a condition characterized by language deficits; 7q36.1-q36.2, 7q36.3, 16p12.1, and 17q22). These results highlight the reproducibility of dyslexia linkage signals, even without formally significant lod scores, and suggest dyslexia predisposing genes with relatively major effects and locus heterogeneity. The largest lod score (2.80) occurred at 17q22 within the MSI2 gene, involved in neuronal stem cell lineage proliferation. Interestingly, the 4q13.1 linkage peak (lod 2.34) occurred immediately upstream of the LPHN3 gene, recently reported both linked and associated with ADHD. Separate analyses of larger pedigrees revealed lods >2.3 at 1-3 regions per family; one family showed strong linkage (lod 2.9) to a known dyslexia locus (18p11) not detected in our overall data, demonstrating the value of analyzing single large pedigrees. Association analysis identified no SNPs with genomewide significance, although a borderline significant SNP (P = 6 × 10 -7 ) occurred at 5q35.1 near FGF18, involved in laminar positioning of cortical neurons during development. We conclude that dyslexia genes with relatively major effects exist, are detectable by linkage analysis despite genetic heterogeneity, and show substantial overlapping predisposition with ADHD and autism.

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Section: Other Regions (Lod 15-23)supporting

confidence: 75%

“…), which found and replicated an association with rs1323381 at 110.10 Mb (although this association was not replicated by Luciano et al . ). A possible regional candidate is AL390170 at 110.93 Mb, an uncharacterized clone highly expressed in fetal and adult brain.…”

Section: Discussionmentioning

confidence: 97%

Dense‐map genome scan for dyslexia supports loci at 4q13, 16p12, 17q22; suggests novel locus at 7q36

Field

Shumansky

Ryan

et al. 2012

Genes Brain and Behavior

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“…2010; Luciano et al . 2007, 2011). Since this time, additional subjects have entered the dataset, primarily recruited at age 12.…”

Section: Resultsmentioning

confidence: 99%

“…Single SNP replication of dyslexia and SLI candidate genes from the literature BATS Our group has already published on candidate dyslexia genes KIAA0319, DYX1C1 and DCDC2 based on targeted genotyping of regions in a smaller dataset than is used here Lind et al 2010;Luciano et al 2007Luciano et al , 2011. Since this time, additional subjects have entered the dataset, primarily recruited at age 12.…”

Section: Gene-based Testsmentioning

confidence: 99%

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A genome‐wide association study for reading and language abilities in two population cohorts

Luciano

Evans

Hansell

et al. 2013

Genes Brain and Behavior

104

132

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Candidate genes have been identified for both reading and language, but most of the heritable variance in these traits remains unexplained. Here, we report a genome-wide association meta-analysis of two large cohorts: population samples of Australian twins and siblings aged 12–25 years (n = 1177 from 538 families), and a younger cohort of children of the UK Avon Longitudinal Study of Parents and their Children (aged 8 and 9 years; maximum n = 5472). Suggestive association was indicated for reading measures and non-word repetition (NWR), with the greatest support found for single nucleotide polymorphisms (SNPs) in the pseudogene, ABCC13 (P = 7.34 × 10−8), and the gene, DAZAP1 (P = 1.32 × 10−6). Gene-based analyses showed significant association (P < 2.8 × 10−6) for reading and spelling with genes CD2L1, CDC2L2 and RCAN3 in two loci on chromosome 1. Some support was found for the same SNPs having effects on both reading skill and NWR, which is compatible with behavior genetic evidence for influences of reading acquisition on phonological-task performance. The results implicate novel candidates for study in additional cohorts for reading and language abilities.

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Genome-wide association scan identifies new variants associated with a cognitive predictor of dyslexia

et al. 2019

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Developmental dyslexia (DD) is one of the most prevalent learning disorders, with high impact on school and psychosocial development and high comorbidity with conditions like attention-deficit hyperactivity disorder (ADHD), depression, and anxiety. DD is characterized by deficits in different cognitive skills, including word reading, spelling, rapid naming, and phonology. To investigate the genetic basis of DD, we conducted a genome-wide association study (GWAS) of these skills within one of the largest studies available, including nine cohorts of reading-impaired and typically developing children of European ancestry (N = 2562–3468). We observed a genome-wide significant effect (p < 1 × 10−8) on rapid automatized naming of letters (RANlet) for variants on 18q12.2, within MIR924HG (micro-RNA 924 host gene; rs17663182 p = 4.73 × 10−9), and a suggestive association on 8q12.3 within NKAIN3 (encoding a cation transporter; rs16928927, p = 2.25 × 10−8). rs17663182 (18q12.2) also showed genome-wide significant multivariate associations with RAN measures (p = 1.15 × 10−8) and with all the cognitive traits tested (p = 3.07 × 10−8), suggesting (relational) pleiotropic effects of this variant. A polygenic risk score (PRS) analysis revealed significant genetic overlaps of some of the DD-related traits with educational attainment (EDUyears) and ADHD. Reading and spelling abilities were positively associated with EDUyears (p ~ [10−5–10−7]) and negatively associated with ADHD PRS (p ~ [10−8−10−17]). This corroborates a long-standing hypothesis on the partly shared genetic etiology of DD and ADHD, at the genome-wide level. Our findings suggest new candidate DD susceptibility genes and provide new insights into the genetics of dyslexia and its comorbities.

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SNP Sets and Reading Ability: Testing Confirmation of a 10-SNP Set in a Population Sample

Cited by 6 publications

References 28 publications

Dense‐map genome scan for dyslexia supports loci at 4q13, 16p12, 17q22; suggests novel locus at 7q36

Dense‐map genome scan for dyslexia supports loci at 4q13, 16p12, 17q22; suggests novel locus at 7q36

A genome‐wide association study for reading and language abilities in two population cohorts

Genome-wide association scan identifies new variants associated with a cognitive predictor of dyslexia

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