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SNP Variations in the 7q33 Region Containing DGKI are Associated with Dyslexia in the Finnish and German Populations

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Abstract

Four genes, DYX1C1, ROBO1, DCDC2 and KIAA0319 have been studied both genetically and functionally as candidate genes for developmental dyslexia, a common learning disability in children. The identification of novel genes is crucial to better understand the molecular pathways affected in dyslectic individuals. Here, we report results from a fine-mapping approach involving linkage and association analysis in Finnish and German dyslexic cohorts. We restrict a candidate region to 0.3 Mb on chromosome 7q33. This region harbours the gene diacylglycerol kinase, iota (DGKI) which contains overlapping haplotypes associated with dyslexia in both Finnish and German sample sets.

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Acknowledgments

We would like to acknowledge the families included in this report, for their participation and the MAF (Mutation Analysis Facility) core facility at Karolinska Insitutet for advice. The study was supported by the Academy of Finland, the Magnus Bergvall’s fund, the Osk. Huttunen Foundation, the Swedish Research Council, the Swedish Royal Bank Tercentennial Fund and the Karolinska Institutet (Sweden), the Finnish Center of Excellence Program (#40166 for 1997–1999, #44858 for 2000–2005 and #213486 for 2006–2011), the Niilo Mäki Foundation and the University of Jyväskylä (Finland). The Departments of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy (University of Munich, Germany) and the Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy (University of Wuerzburg, Germany) were supported by funds DFG-WA715/7-1 and RE 471/15-1 for this study.

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The authors declare that there are no conflicts of interests.

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Correspondence to Hans Matsson or Myriam Peyrard-Janvid.

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Edited by Elena Grigorenko and Brett Miller.

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Matsson, H., Tammimies, K., Zucchelli, M. et al. SNP Variations in the 7q33 Region Containing DGKI are Associated with Dyslexia in the Finnish and German Populations. Behav Genet 41, 134–140 (2011). https://doi.org/10.1007/s10519-010-9431-4

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  • DOI: https://doi.org/10.1007/s10519-010-9431-4

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