부산대학교 도서관

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 deletioncompound short tandem repeat (STR) polymorphism in intron 2 of DCDC2as 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 DCDC2locus. We observed no significant deviation from random transmission, neither for the deletion nor for the alleles of the compound STR. We also did not find the deletion or any of the STR 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 variants in DCDC2conferring susceptibility to dyslexia in our sample remains to be identified.