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. 2001 Nov;69(5):1062-7.
doi: 10.1086/324191. Epub 2001 Oct 2.

Excess of twins among affected sibling pairs with autism: implications for the etiology of autism

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Excess of twins among affected sibling pairs with autism: implications for the etiology of autism

D A Greenberg et al. Am J Hum Genet. 2001 Nov.

Abstract

It is widely accepted that genes play a role in the etiology of autism. Evidence for this derives, in part, from twin data. However, despite converging evidence from gene-mapping studies, aspects of the genetic contribution remain obscure. In a sample of families selected because each had exactly two affected sibs, we observed a remarkably high proportion of affected twin pairs, both MZ and DZ. Of 166 affected sib pairs, 30 (12 MZ, 17 DZ, and 1 of unknown zygosity) were twin pairs. Deviation from expected values was statistically significant (P<10(-6) for all twins); in a similarly ascertained sample of individuals with type I diabetes, there was no deviation from expected values. We demonstrate that to ascribe the excess of twins with autism solely to ascertainment bias would require very large ascertainment factors; for example, affected twin pairs would need to be, on average, approximately 10 times more likely to be ascertained than affected non-twin sib pairs (or 7 times more likely if "stoppage" plays a role). Either risk factors (related to twinning or to fetal development) or other factors (genetic or nongenetic) in the parents may contribute to autism.

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References

Electronic-Database Information

    1. Online Mendelian Inheritance in Man (OMIM), http://www.ncbi.nlm.nih.gov/Omim (for autism [MIM 209850])

References

    1. Ashley-Koch A, Wolpert CM, Menold MM, Zaeem L, Basu S, Donnelly SL, Ravan SA, Powell CM, Qumsiyeh MB, Aylsworth AS, Vance JM, Gilbert JR, Wright HH, Abramson RK, DeLong GR, Cuccaro ML, Pericak-Vance MA (1999) Genetic studies of autistic disorder and chromosome 7. Genomics 61:227–236 - PubMed
    1. Auranen M, Nieminen T, Majuri S, Vanhala R, Peltonen L, Järvelä I (2000) Analysis of autism susceptibility gene loci on chromosomes 1p, 4p, 6q, 7q, 13q, 15q, 16q, 17q, 19q and 22q in Finnish multiplex families. Mol Psychiatry 5:320–322 - PubMed
    1. Bailey A, Le Couteur A, Gottesman I, Bolton P, Simonoff E, Yuzda E, Rutter M (1995) Autism as a strongly genetic disorder: evidence from a British twin study. Psychol Med 25:63–77 - PubMed
    1. Barrett S, Beck JC, Bernier R, Bisson E, Braun TA, Casavant TL, Childress D, et al (1999) An autosomal genomic screen for autism: collaborative linkage study of autism. Am J Med Genet 88:609–615 - PubMed
    1. Buxbaum JD, Silverman JM, Smith CJ, Kilifarski M, Reichert J, Hollander E, Lawlor BA, Fitzgerald M, Greenberg DA, Davis KL (2001) Evidence for a susceptibility gene for autism on chromosome 2 and for genetic heterogeneity. Am J Hum Genet 68:1514–1520 - PMC - PubMed

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