Results of synesthetes’ grapheme-color correspondences indeed revealed that more similarly shaped graphemes corresponded with more similar synesthetic colors, with stronger effects observed in individuals with more intense synesthetic experiences

(projector synesthetes). These results support the CCT model of synesthesia, implicate early perceptual mechanisms as driving factors in the elicitation of synesthetic hues, and further highlight the relationship between conceptual and perceptual factors in this phenomenon. (C) 2011 Elsevier Ltd. All rights reserved.”
“Background Large, rare chromosomal deletions and duplications known as copy number variants (CNVs) have been implicated in neurodevelopmental disorders similar to attention-deficit find more hyperactivity disorder (ADHD). We aimed to establish whether burden of CNVs was increased in ADHD, and to investigate whether identified CNVs were enriched for loci previously identified in autism and schizophrenia.

Methods We selleck inhibitor undertook a genome-wide analysis of CNVs in 410 children with ADHD and 1156 unrelated ethnically matched controls from the 1958 British Birth Cohort. Children of white UK origin, aged 5-17 years, who met diagnostic criteria for ADHD or

hyperkinetic disorder, but not schizophrenia and autism, were recruited from community child psychiatry and paediatric outpatient clinics. Single nucleotide polymorphisms (SNPs) were genotyped in the ADHD and control groups with two arrays; CNV analysis was limited to SNPs common to both arrays and included only samples with high-quality data. CNVs in the ADHD group were validated with comparative genomic hybridisation. We assessed the genome-wide heptaminol burden of large (>500 kb), rare (<1% population frequency) CNVs according to the average number of CNVs per sample, with significance assessed via permutation. Locus-specific tests of association were undertaken for test regions defined for all identified CNVs and for 20 loci implicated in autism or schizophrenia.

Findings were replicated in 825 Icelandic patients with ADHD and 35 243 Icelandic controls. Findings Data for full

analyses were available for 366 children with ADHD and 1047 controls. 57 large, rare CNVs were identified in children with ADHD and 78 in controls, showing a significantly increased rate of CNVs in ADHD (0.156 vs 0.075; p=8.9×10(-5)). This increased rate of CNVs was particularly high in those with intellectual disability (0.424; p=2.0×10(-6)), although there was also a significant excess in cases with no such disability (0.125, p=0.0077). An excess of chromosome 16p13.11 duplications was noted in the ADHD group (p=0.0008 after correction for multiple testing), a finding that was replicated in the Icelandic sample (p=0.031). CNVs identified in our ADHD cohort were significantly enriched for loci previously reported in both autism (p=0.0095) and schizophrenia (p=0.010).