Abstract

Dyslexia is a hereditary neurological disorder that manifests as an unexpected difficulty in learning to read despite adequate intelligence, education, and normal senses. The prevalence of dyslexia ranges from 3 to 15% of the school aged children. Many genetic studies indicated that loci on 6p21.3, 15q15-21, and 18p11.2 have been identified as promising candidate gene regions for dyslexia. Recently, it has been suggested that allelic variants of gene, DYX1C1 influence dyslexia. In the present study, exon 2 and 10 of DYX1C1 has been analyzed to verify whether these single nucleotide polymorphisms (SNPs) influence dyslexia, in our population. Our study identified 4 SNPs however, none of these SNPS were found to be significantly associated with dyslexia suggesting DYX1C1 allelic variants are not associated with dyslexia.

Highlights

  • Developmental dyslexia is a hereditary neurological disorder that manifests as a persistent difficulty in learning to read and spell in children with otherwise normal intellectual functioning and educational opportunities. [1] Prevalence of dyslexia in school children has been found to be 3-17.5%.[2]

  • Eight single nucleotide polymorphisms (SNPs) are located in DYX1C1, of them two SNPs -3G>A and 1249C>T was reported to be associated with dyslexia. -3G>A is located in the binding sequence of the transcription factors and it was reported that transcriptional activator, Elk-1 has been associated with learning in rats

  • SNP 1249C>T brings a functional effect by truncating the protein

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Summary

Introduction

Developmental dyslexia is a hereditary neurological disorder that manifests as a persistent difficulty in learning to read and spell in children with otherwise normal intellectual functioning and educational opportunities. [1] Prevalence of dyslexia in school children has been found to be 3-17.5%.[2]. One of the possible candidate genes, which influence dyslexia, is DYX1C1 which is near DYX1 locus on chromosome 15q21. Sequence analysis of DYX1C1 shows eight single nucleotide polymorphisms (SNPs), of them two SNPs, -3G>A and 1249G>T are functionally important and influences dyslexia.[10]

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