A genomic screen of autism: evidence for a multilocus etiology. |
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| Authors: | N Risch D Spiker L Lotspeich N Nouri D Hinds J Hallmayer L Kalaydjieva P McCague S Dimiceli T Pitts L Nguyen J Yang C Harper D Thorpe S Vermeer H Young J Hebert A Lin J Ferguson C Chiotti S Wiese-Slater T Rogers B Salmon P Nicholas P B Petersen C Pingree W McMahon D L Wong L L Cavalli-Sforza H C Kraemer R M Myers |
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| Affiliation: | Department of Genetics, M322, Stanford University School of Medicine, Stanford, CA 94305-5120, USA. Risch@lahmed.stanford.edu |
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| Abstract: | We have conducted a genome screen of autism, by linkage analysis in an initial set of 90 multiplex sibships, with parents, containing 97 independent affected sib pairs (ASPs), with follow-up in 49 additional multiplex sibships, containing 50 ASPs. In total, 519 markers were genotyped, including 362 for the initial screen, and an additional 157 were genotyped in the follow-up. As a control, we also included in the analysis unaffected sibs, which provided 51 discordant sib pairs (DSPs) for the initial screen and 29 for the follow-up. In the initial phase of the work, we observed increased identity by descent (IBD) in the ASPs (sharing of 51.6%) compared with the DSPs (sharing of 50.8%). The excess sharing in the ASPs could not be attributed to the effect of a small number of loci but, rather, was due to the modest increase in the entire distribution of IBD. These results are most compatible with a model specifying a large number of loci (perhaps >/=15) and are less compatible with models specifying
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