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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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Title: SNP Variations in the 7q33 Region Containing DGKI are Associated with Dyslexia in the Finnish and German Populations.
Authors: Matsson, Hans, Tammimies, Kristiina, Zucchelli, Marco, Anthoni, Heidi, Onkamo, Päivi, Nopola-Hemmi, Jaana, Lyytinen, Heikki, Leppanen, Paavo H. T., Neuhoff, Nina, Warnke, Andreas, Schulte-Körne, Gert, Schumacher, Johannes, Nöthen, Markus M., Kere, Juha, Peyrard-Janvid, Myriam
Source: Behavior Genetics. Jan2011, Vol. 41 Issue 1, p134-140. 7p. 1 Diagram, 1 Chart, 1 Graph.
Subjects: Dyslexia, Genes, Learning disability genetics, Linkage (Genetics), Reading disability, Developmental disabilities
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. [ABSTRACT FROM AUTHOR]
Copyright of Behavior Genetics is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: SNP Variations in the 7q33 Region Containing DGKI are Associated with Dyslexia in the Finnish and German Populations.
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  Data: <searchLink fieldCode="DE" term="%22Dyslexia%22">Dyslexia</searchLink><br /><searchLink fieldCode="DE" term="%22Genes%22">Genes</searchLink><br /><searchLink fieldCode="DE" term="%22Learning+disability+genetics%22">Learning disability genetics</searchLink><br /><searchLink fieldCode="DE" term="%22Linkage+%28Genetics%29%22">Linkage (Genetics)</searchLink><br /><searchLink fieldCode="DE" term="%22Reading+disability%22">Reading disability</searchLink><br /><searchLink fieldCode="DE" term="%22Developmental+disabilities%22">Developmental disabilities</searchLink>
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  Data: 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. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Behavior Genetics is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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