Genome-wide copy number scan identifies disruption of PCDH11X in developmental dyslexia

Developmental Dyslexia (DD) is a complex heritable disorder with unexpected difficulty in learning to read and spell despite adequate intelligence, education, environment, and normal senses. We performed a whole genome Copy Number Variations (CNV) scan on 11 dyslexic families consisting of 14 dyslexic subjects and 24 non dyslexic members using 1.8 million combined SNP and CNV markers. We found CNVs affecting protocadherin genes in six dyslexics from three families, while none among the non-dyslexic control members showed any CNV in protocadherins. We identified duplications in five cases and a deletion in one case in Xq21.3 region bearing PCDH11X. Unequal recombination between the X-transposed Region (XTR) of Yp11.2 and the X chromosome might be causing these structural changes. PCDH11X, expressed in brain is implicated in cell–cell communication, verbal ability, cerebral asymmetry and dendritic synaptic plasticity may be regarded as a new candidate gene for dyslexia

Development of rapid automatized naming (ran) in simultaneous kannada-english biliterate children

RAN tests were administered to 600 typically developing children, 60 each from grade level one through grade ten (30 boys and 30 girls), who learn two distinct languages, English and Kannada simultaneously from the very first grade. The overall results were in accordance with similar previous studies in English and other European languages. The developmental trajectories were similar across the languages to a large extent; but the results also showed some differences across languages with respect to synchrony between the measures and the overall naming speed. Though some of the differences could be ascribed to the bilingual/biliterate culture and language use, there are enough scopes for future researches to examine these issues

Family-based genome-wide copy number scan identifies five new genes of dyslexia involved in dendritic spinal plasticity

Genome-wide screening for copy number variations (CNVs) in ten Indian dyslexic families revealed the presence of five de novo CNVs in regions harboring GABARAP, NEGR1, ACCN1, DCDC5, and one in already known candidate gene CNTNAP2. These genes are located on regions of chromosomes 17p13.1, 1p31.1, 17q11.21, 11p14.1 and 7q35, respectively, and are implicated in learning, cognition and memory processes through dendritic spinal plasticity, though not formally associated with dyslexia. Molecular network analysis of these and other dyslexia-related module genes suggests them to be associated with synaptic transmission, axon guidance and cell adhesion. Thus, we suggest that dyslexia may also be caused by neuronal disconnection in addition to the earlier view that it is due to neuronal migrational disorder