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Investigation of the DCDC2 intron 2 deletion/compound short tandem repeat polymorphism in a large German dyslexia sample

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons80450

Mueller-Myhsok,  B.
AG Müller-Myhsok, Bertram, Florian Holsboer (Direktor), Max Planck Institute of Psychiatry, Max Planck Society;

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Zitation

Ludwig, K. U., Schumacher, J., Schulte-Körne, G., König, I. R., Warnke, A., Plume, E., et al. (2008). Investigation of the DCDC2 intron 2 deletion/compound short tandem repeat polymorphism in a large German dyslexia sample. Psychiatric Genetics, 18(6), 310-312.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000E-9363-2
Zusammenfassung
Dyslexia is a complex disorder manifested by difficulties in learning to read and spell despite conventional instruction, adequate intelligence and sociocultural opportunity. It is among the most common neurodevelopmental disorders with a prevalence of 5-12%. The dyslexia susceptibility locus 2 on chromosome 6p21-p22 is one of the best-replicated linkage regions in dyslexia. On the basis of systematic linkage disequilibrium studies, the doublecortin domain containing protein 2 gene (DCDC2) was identified as a strong candidate gene in this region. Data from a US study have suggested a complex deletion/compound short tandem repeat (STR) polymorphism in intron 2 of DCDC2 as the causative mutation. In this study, we analyzed this polymorphism in 396 German dyslexia trios which included 376 trios previously providing strong support for the DCDC2 locus. We observed no significant deviation from random transmission, neither for the deletion nor for the alleles of the compound STIR. We also did not find the deletion or any of the STIR alleles to be in linkage disequilibrium with the 2-marker haplotype, which was associated with dyslexia in our sample. We thus conclude that the causative variant/s in DCDC2 conferring susceptibility to dyslexia in our sample remain/s to be identified. Psychiatr Genet 18:310-312 (C) 2008 Wolters Kluwer Health / Lippincott Williams & Wilkins.