title: No Evidence of Antibodies against GAD65 and Other Specific Antigens in Children with Autism.
abstract: BACKGROUND
  The presence of autoantibodies has been proposed as evidence for a role of autoimmunity in autism. This report investigates the prevalence of autoantibodies in children with autism using the luciferase immunoprecipitation systems (LIPS) immunoassay technology. A panel of autoantibody targets against several known and candidate neurological autoantigens, autoimmune-associated autoantigens and viruses was employed.
  
  
  METHODS
  Serological analysis was performed on typically developing children (n = 55), developmentally delayed children without autism (n = 24) and children diagnosed with autism (n=104). Autoantibodies were measured against glutamic acid decarboxylase-65 (GAD65), a CNS autoantigen proposed to be associated with autism and against Ro52, glial fibrillary acidic protein, tyrosine hydroxylase, aquaporin-4, and gamma-enolase, the mouse mammary tumor virus and the xenotropic murine leukemia virus. Antibody levels and seropositivity prevalence were analyzed for statistically significant differences between the three groups.
  
  
  RESULTS
  The majority of the children (98%) were seronegative for all targets in the antigen panel. No GAD65 seropositive children were detected in the cohort. Several low level seropositive sera against several of the protein targets were identified in isolated children in each of the three groups, but there was no difference in prevalence.
  
  
  CONCLUSIONS
  Using this panel of antigens and a sensitive, robust assay, no evidence of unusual immunoreactivity was detected in children with autism, providing evidence against a role of autoimmunity against several previously implicated proteins in autism spectrum disorder pathogenesis.
  
  
  CONCLUSIONS
  The idea that autoantibodies represent an underlying cause or are biomarkers for autism pathophysiology is not supported by this report.
authors.affiliation: Pediatrics and Developmental Branch, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD.
authors.forename: Simran
authors.initials: S
authors.lastname: Kalra
authors.affiliation: Dental Clinical Research Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD.
authors.forename: Peter D
authors.initials: PD
authors.lastname: Burbelo
authors.affiliation: Department of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD.
authors.forename: Ahmad
authors.initials: A
authors.lastname: Bayat
authors.affiliation: Department of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD.
authors.forename: Kathryn H
authors.initials: KH
authors.lastname: Ching
authors.affiliation: Pediatrics and Developmental Branch, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD.
authors.forename: Audrey
authors.initials: A
authors.lastname: Thurm
authors.affiliation: Department of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Iadarola
authors.affiliation: Pediatrics and Developmental Branch, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD.
authors.forename: Susan E
authors.initials: SE
authors.lastname: Swedo