Journal
NATURE
Volume 459, Issue 7246, Pages 528-533Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature07999
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Funding
- National Institute of Mental Health [1U24MH081810]
- National Institute of Child Health and Human Development [NO1-HD-4-3368, NO1-HD-4-3383]
- Institutional Development Award
- Margaret Q. Landenberger Foundation
- Cotswold Foundation [UL1-RR024134-03]
- Mental Retardation and Developmental Disability Research Center
- Beatrice and Stanley A. Seaver Foundation
- Department of Veterans Affairs
- NIH [MH64547, HD055782-01, MH0666730, MH061009, NS049261, HD055751, MH69359, M01-RR00064, MH081754, HD055784, NS26630, NS36768, MH080647]
- Autism Genome Project Consortium
- Autism Speaks
- Medical Research Council (UK) and the Health Research Board (Ireland)
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Autism spectrum disorders (ASDs) represent a group of childhood neurodevelopmental and neuropsychiatric disorders characterized by deficits in verbal communication, impairment of social interaction, and restricted and repetitive patterns of interests and behaviour. To identify common genetic risk factors underlying ASDs, here we present the results of genome-wide association studies on a cohort of 780 families (3,101 subjects) with affected children, and a second cohort of 1,204 affected subjects and 6,491 control subjects, all of whom were of European ancestry. Six single nucleotide polymorphisms between cadherin 10 (CDH10) and cadherin 9 (CDH9)-two genes encoding neuronal cell-adhesion molecules-revealed strong association signals, with the most significant SNP being rs4307059 (P = 3.4 x 10(-8), odds ratio = 1.19). These signals were replicated in two independent cohorts, with combined P values ranging from 7.4 x 10(-8) to 2.1 x 10(-10). Our results implicate neuronal cell-adhesion molecules in the pathogenesis of ASDs, and represent, to our knowledge, the first demonstration of genome-wide significant association of common variants with susceptibility to ASDs.
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