The role of gene DCDC2 in German dyslexics

Wilcke, Arndt; Weissfuss, Jana; Kirsten, Holger; Wolfram, Grit; Boltze, Johannes; Ahnert, Peter

doi:10.1007/s11881-008-0020-7

Cited by 67 publications

(79 citation statements)

References 33 publications

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“…Replication of this SNP, along with expression and/or sequencing analyses to uncover its associated functional effects, would be desirable. We did not find significant support for association of reading and spelling with rs793862, the most widely genotyped polymorphism in DCDC2 association studies; though we did observe the same at-risk allele as in earlier studies 10,11,36,37 (the T-allele conferred a reading disadvantage of just 0.02 SD). Contradictory findings have been reported for this SNP: from nominally significant associations, 8,9 to associations specific only in the most severely affected families, 10 to the reverse effect (a nominally significant association in independent UK samples that disappeared when the sample was restricted to individuals with severe spelling difficulties 7 ), to no support for association of rs793862 to dyslexia in a cohort of US families.…”

Section: Discussioncontrasting

confidence: 97%

Dyslexia and DCDC2: normal variation in reading and spelling is associated with DCDC2 polymorphisms in an Australian population sample

et al. 2010

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The 6p21-p22 chromosomal region has been identified as a developmental dyslexia locus both in linkage and association studies, the latter generating evidence for the doublecortin domain containing 2 (DCDC2) as a candidate gene at this locus (and also for KIAA0319). Here, we report an association between DCDC2 and reading and spelling ability in 522 families of adolescent twins unselected for reading impairment. Family-based association was conducted on 21 single nucleotide polymorphisms (SNPs) in DCDC2 using quantitative measures of lexical processing (irregular-word reading), phonological decoding (non-word reading) and spelling-based measures of dyslexia derived from the Components of Reading Examination test. Significant support for association was found for rs1419228 with regular-word reading and spelling (P¼0.002) as well as irregular-word reading (P¼0.004), whereas rs1091047 was significantly associated (P¼0.003) with irregular-word reading (a measure of lexical storage). Four additional SNPs (rs9467075, rs9467076, rs7765678 and rs6922023) were nominally associated with reading and spelling. This study provides support for DCDC2 as a risk gene for reading disorder, and suggests that this risk factor acts on normally varying reading skill in the general population.

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Section: Discussioncontrasting

confidence: 97%

Dyslexia and DCDC2: normal variation in reading and spelling is associated with DCDC2 polymorphisms in an Australian population sample

et al. 2010

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“…Most of the genetic associations with dyslexia cluster around the 5' end of the KIAA0319 gene and generally show the same allelic trends across independent studies (Francks et al, 2004, Cope et al, 2005Schumacher et al, 2007;Luciano et al, 2007;Paracchini et al, 2008;Couto et al, 2009;Dennis et al, 2009;Wilcke et al, 2009). Francks et al (2004) identified 1 main RD risk haplotype comprising 3 SNPs (rs4504469, rs2038137, and rs2143340) with a frequency of 12% in families from the United Kingdom and the United States.…”

Section: Introductionmentioning

confidence: 73%

“…Ludwig et al (2008) used both categorically and quantitatively related traits to investigate the association between RD and DCDC2 intron 2 deletion and short tandem repeat (STR) variants, but did not detect a significant association between RD and these genetic variants. In contrast, Wilcke et al (2009), studying an independent German sample, reported evidence for an association between the DCDC2 intron 2 deletion variant and a dyseidetic diagnostic subtype characterized by major impairment of visual perception. Lind et al (2010) recently reported a study supporting an association of 2 SNPs in DCDC2 with quantitative measures in Australian families that were unselected for reading impairment.…”

Section: Introductionmentioning

confidence: 92%

Study of candidate genes for dyslexia in Brazilian individuals

Svidnicki¹,

Salgado²,

Lima³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Dyslexia or reading disability (RD) is the most common childhood learning disorder and a significantly heritable trait. Many recent studies have investigated the genetic basis of dyslexia, and several candidate genes have been proposed. Among these, DCDC2 and KIAA0319 have emerged as the strongest candidate genes for dyslexia; however studies have not provided uniformly supportive results. The aim of this study was to assess the contribution of proposed candidate genes to the molecular etiology of dyslexia in a Brazilian sample. Large deletions and duplications in the candidate genes DCDC2, KIAA0319, and ROBO1 were investigated in 51 dyslexic subjects. Furthermore, a family-based association study was performed to investigate whether associations observed in other populations with variants in the Dyslexia candidate genes DCDC2 and KIAA0319 genes were reproducible in Brazilian dyslexic individuals. Our analysis did not detect any deletions or duplications in the genes studied, and we found no evidence that the allelic variants in the two candidate genes were significantly associated with RD in our sample. Our data do not support a role of the DCDC2/KIAA0319 locus in influencing dyslexia as a categorical trait. Given the genetic complexity of dyslexia, it is plausible that both genes contribute to an increased risk, but the relative influence of these 2 genes on RD varies in different study samples, and/or depends on analytical approaches.

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“…Table 5 Genes with Known Function from the List of Best Hits in Table 2. DCDC2 is thought to play a role in neuronal migration, and has been associated with dyslexia in multiple independent studies (e.g., Meng et al, 2005;Schumacher et al, 2006;Wilcke et al, 2009) (p values = .0003, .004, and <.05 respectively). It has been associated with variation in reading and spelling ability in a general population (p values <.001) (Lind et al, 2010), with inattention and hyperactivity/impulsivity symptoms of ADHD (Couto et al, 2009), and with the distribution of grey matter in language-related brain regions in healthy individuals (p < .01 for volumetric differences between genotype groups) (Meda et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Whole genome association scan for genetic polymorphisms influencing information processing speed

Luciano

Hansell

Lahti

et al. 2011

Biological Psychology

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Processing speed is an important cognitive function that is compromised in psychiatric illness (e.g., schizophrenia, depression) and old age; it shares genetic background with complex cognition (e.g., working memory, reasoning). To find genes influencing speed we performed a genome-wide association scan in up to three cohorts: Brisbane (mean age 16 years; N = 1659); LBC1936 (mean age 70 years, N = 992); LBC1921 (mean age 82 years, N = 307), and; HBCS (mean age 64 years, N = 1080). Meta-analysis of the common measures highlighted various suggestively significant (p < 1.21 × 10 −5 ) SNPs and plausible candidate genes (e.g., TRIB3). A biological pathways analysis of the speed factor identified two common pathways from the KEGG database (cell junction, focal adhesion) in two cohorts, while a pathway analysis linked to the GO database revealed common pathways across pairs of speed measures (e.g., receptor binding, cellular metabolic process). These highlighted genes and pathways will be able to inform future research, including results for psychiatric disease. KeywordsInformation processing speed; Cognitive ability; Genes; Biological pathways © 2010 Elsevier B.V. All rights reserved. * Corresponding author at: Psychology, University of Edinburgh, 7 George Square, Edinburgh EH8 9JZ, UK. Tel.: +44 131 6 51 5040; fax: +44 131 650 8405. michelle.luciano@ed.ac.uk. . 1 These authors contributed equally to this work. Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi: 10.1016/j.biopsycho.2010.11.008. Europe PMC Funders GroupAuthor Manuscript Biol Psychol. Author manuscript; available in PMC 2012 April 04. Published in final edited form as:Biol Psychol. 2011 March ; 86(3): 193-202. doi:10.1016/j.biopsycho.2010 Europe PMC Funders Author Manuscripts Europe PMC Funders Author ManuscriptsInformation processing speed is considered a lower level cognitive process, although it shares a large portion of its genetic variance with higher order abilities (e.g., reasoning, working memory) (Luciano et al., 2003;Neubauer, 1997). It is a cognitive domain that is particularly prone to deterioration with ageing (Salthouse, 1996); for example, simple reaction time (RT) slows at around 50 years of age and choice RT slows throughout the adult range (Der and Deary, 2006). However, similar to complex cognition with which it is correlated, the genes influencing speed are expected to be stable across the lifespan (Lyons et al., 2009). Speed is affected (slowed) in psychiatric conditions such as schizophrenia, depression and substance use disorder (Andersson et al., 2010;Jahshan et al., 2009) and RT has even been shown to account for the relationship between IQ and mortality in a cohort followed up until age 70 (Deary and Der, 2005;Latvala et al., 2009). It is therefore an important trait to understand, and in this study, we aim to locate genes influencing chronometric and psychometric processing speed measures via genome wide association. These genes may underlie comple...

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The role of gene DCDC2 in German dyslexics

Cited by 67 publications

References 33 publications

Dyslexia and DCDC2: normal variation in reading and spelling is associated with DCDC2 polymorphisms in an Australian population sample

Dyslexia and DCDC2: normal variation in reading and spelling is associated with DCDC2 polymorphisms in an Australian population sample

Study of candidate genes for dyslexia in Brazilian individuals

Whole genome association scan for genetic polymorphisms influencing information processing speed

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