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We searched for linkage disequilibrium (LD) in 137 triads with dyslexia, using markers that span the most-replicated dyslexia susceptibility region on 6p21-p22, and found association between the disease and markers within the VMP/DCDC2/KAAG1 locus. Detailed refinement of the LD region, involving sequencing and genotyping of additional markers, showed significant association within DCDC2 in single-marker and haplotype analyses. The association appeared to be strongest in severely affected patients. In a second step, the study was extended to include an independent sample of 239 triads with dyslexia, in which the association--in particular, with the severe phenotype of dyslexia--was confirmed. Our expression data showed that DCDC2, which contains a doublecortin homology domain that is possibly involved in cortical neuron migration, is expressed in the fetal and adult CNS, which--together with the hypothesized protein function--is in accordance with findings in dyslexic patients with abnormal neuronal migration and maturation.

Original publication




Journal article


American journal of human genetics

Publication Date





52 - 62


Institute of Human Genetics, University of Bonn, Bonn, Germany.


Central Nervous System, Chromosomes, Human, Pair 6, Humans, Dyslexia, Genetic Predisposition to Disease, Microtubule-Associated Proteins, Nerve Tissue Proteins, DNA Primers, Genetic Markers, Blotting, Northern, Sequence Analysis, DNA, Base Sequence, Genotype, Haplotypes, Linkage Disequilibrium, Phenotype, Gene Components, Molecular Sequence Data, Germany