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No evidence for linkage of liability to autism toHOXA1 in a sample from the CPEA network

✍ Scribed by Devlin, Bernie ;Bennett, Pamela ;Cook,, Edwin H. ;Dawson, Geraldine ;Gonen, David ;Grigorenko, Elena L. ;McMahon, William ;Pauls, David ;Smith, Moyra ;Spence, M. Anne ;Schellenberg, Gerard D. ;,

Publisher: John Wiley and Sons
Year: 2002
Tongue: English
Weight: 79 KB
Volume: 114
Category: Article
ISSN: 0148-7299
DOI: 10.1002/ajmg.10603

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✦ Synopsis

A recent study by Ingram et al. [2000b: Teratology 62:393-405] suggests a (His)73(Arg) polymorphism (A:G) in HOXA1 contributes substantially to a liability for autism. Using 68 individuals diagnosed with Autism Spectrum Disorders, they found a significant dearth of G homozygotes and biased transmission of G alleles from parents to affected offspring, especially from mothers. Because the connection between HOXA1 and liability to autism is compelling, we attempted to replicate their finding using a larger, independent sample from the Collaborative Programs of Excellence in Autism (CPEA) network. In our data, genotype frequencies conform to Hardy-Weinberg equilibrium; allele transmissions meet Mendelian expectations; and there is no obvious sex-biased allele transmission. Based on our sample size, calculations suggest that we would have at least 95% power to detect linkage and association even if the A:G polymorphism were to account for only 1% of the heritability of autism. Therefore, although we cannot exclude the possibility that the samples in the two studies are intrinsically different, our data from our sample argue against a major role for HOXA1 (His)73(Arg) in liability to autism.

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