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Alleles of a reelin CGG repeat do not convey liability to autism in a sample from the CPEA network.

A recent study by Persico et al. [2001: Mol Psychiatry 6:150-159] suggests alleles of a CGG polymorphism, just 5' of the reelin gene (RELN) initiator codon, confer liability for autism, especially alleles bearing 11 or more CGG repeats (long alleles). The association is consistent across both a case-control and family-based sample. We attempted to replicate their finding using a larger, independent family-based sample from the NIH Collaborative Programs of Excellence in Autism (CPEA) Network. In our data, allele transmissions to individuals with autism versus unaffected individuals are unbiased, both when alleles are classified by repeat length and when they are classified into long/short categories. Because of the apparent linkage of autism to chromosome 7q, particularly related to the development of language, we also evaluate the relationship between Reelin alleles and the age at which autism subjects use their first word or first phrase. Neither is significantly associated with Reelin alleles. Our results are not consistent with a major role for Reelin alleles in liability to autism.

Pubmed ID: 15048647


  • Devlin B
  • Bennett P
  • Dawson G
  • Figlewicz DA
  • Grigorenko EL
  • McMahon W
  • Minshew N
  • Pauls D
  • Smith M
  • Spence MA
  • Rodier PM
  • Stodgell C
  • Schellenberg GD
  • CPEA Genetics Network


American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics

Publication Data

April 1, 2004

Associated Grants

  • Agency: NCRR NIH HHS, Id: M01 RR 00064
  • Agency: NIMH NIH HHS, Id: MH 57881
  • Agency: NICHD NIH HHS, Id: P01 HD 34565
  • Agency: NICHD NIH HHS, Id: P01 HD 35476
  • Agency: NIMH NIH HHS, Id: R01 MH057881

Mesh Terms

  • Alleles
  • Autistic Disorder
  • Case-Control Studies
  • Cell Adhesion Molecules, Neuronal
  • Extracellular Matrix Proteins
  • Genetic Predisposition to Disease
  • Humans
  • Linkage Disequilibrium
  • Nerve Tissue Proteins
  • Serine Endopeptidases
  • Trinucleotide Repeats