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Am J Hum Genet. 2006 Jan;78(1):52-62. Epub 2005 Nov 17.

Strong genetic evidence of DCDC2 as a susceptibility gene for dyslexia.

Author information

1
Institute of Human Genetics, University of Bonn, Bonn, Germany. johannes.schumacher@uni-bonn.de.

Abstract

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.

PMID:
16385449
PMCID:
PMC1380223
DOI:
10.1086/498992
[Indexed for MEDLINE]
Free PMC Article

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