title: Genes controlling affiliative behavior as candidate genes for autism.
abstract: BACKGROUND
  Autism spectrum disorders (ASD) are neurodevelopmental disorders of complex etiology, with a recognized substantial contribution of heterogeneous genetic factors; one of the core features of ASD is a lack of affiliative behaviors.
  
  
  METHODS
  On the basis of the existing literature, in this study we examined the hypothesis of allelic associations between genetic variants in six genes involved in control of maternal and affiliative behaviors (OXT, OXTR, PRL, PRLR, DbetaH, and FOSB). One hundred and seventy-seven probands with ASD from 151 families (n = 527) were assessed with a set of related instruments capturing multiple facets of ASD. Multivariate and univariate phenotypes were constructed from these assessments and subjected to genetic linkage and association analyses with PBAT and FBAT software.
  
  
  RESULTS
  The resulting pattern of findings, in general, confirmed the hypotheses of the significance of the genes involved in the development of affiliative behaviors in the manifestation of ASD (p values ranging from .000005 to .05); statistically speaking, the strongest results were obtained for allelic associations with the PRL, PRLR, and OXTR genes.
  
  
  CONCLUSIONS
  These preliminary data provide additional support for the hypothesis that the allelic variants of genes necessary for the development of species-typical affiliative behaviors are associated with ASD. Independent replication of these findings is needed and studies of other genes associated with affiliative behaviors are indicated.
authors.affiliation: Department of Statistics, Department of Epidemiology and PublicHealth, Yale University, NewHaven, CT 06519-1124, USA.
authors.forename: Carolyn M
authors.initials: CM
authors.lastname: Yrigollen
authors.forename: Summer S
authors.initials: SS
authors.lastname: Han
authors.forename: Anna
authors.initials: A
authors.lastname: Kochetkova
authors.forename: Tammy
authors.initials: T
authors.lastname: Babitz
authors.forename: Joseph T
authors.initials: JT
authors.lastname: Chang
authors.forename: Fred R
authors.initials: FR
authors.lastname: Volkmar
authors.forename: James F
authors.initials: JF
authors.lastname: Leckman
authors.forename: Elena L
authors.initials: EL
authors.lastname: Grigorenko
mesh_terms: D000704:Analysis of Variance; D020817:Asperger Syndrome / Q000235:genetics; D001321:Autistic Disorder / Q000235:genetics* / Q000503:physiopathology*; D001519:Behavior / Q000502:physiology*; D002648:Child; D004299:Dopamine beta-Hydroxylase / Q000235:genetics; D005192:Family Health; D005260:Female; D008040:Genetic Linkage; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D005838:Genotype; D006801:Humans; D008297:Male; D009935:Organizational Affiliation; D010121:Oxytocin / Q000235:genetics; D011388:Prolactin / Q000235:genetics; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics; D018045:Receptors, Oxytocin / Q000235:genetics; D011981:Receptors, Prolactin / Q000235:genetics
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D018045:Receptors, Oxytocin; D011981:Receptors, Prolactin; D010121:Oxytocin; D011388:Prolactin; D004299:Dopamine beta-Hydroxylase