Evidence map›Paper›PMID 26366376›Full record

ArticleBBA clinical2015

No Evidence of Antibodies against GAD65 and Other Specific Antigens in Children with Autism.

Simran Kalra, Peter D Burbelo, Ahmad Bayat, Kathryn H Ching, Audrey Thurm, Michael J Iadarola, Susan E Swedo

Open access · hybridAbstract read
In one paragraph

Article in BBA clinical, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Simran KalraPediatrics and Developmental Branch, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD.
Peter D BurbeloDental Clinical Research Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD.
Ahmad BayatDepartment of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD.
Kathryn H ChingDepartment of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD.
Audrey ThurmPediatrics and Developmental Branch, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD.
Michael J IadarolaDepartment of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD.
Susan E SwedoPediatrics and Developmental Branch, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD.
National Institutes of Health Clinical Center · USNational Institute of Dental and Craniofacial Research · US

Funding

Clinical and Behavioral Phenotyping of Autism and Related DisordersZIAMH002868 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI SWEDO, SUSAN · 2009 to 2017
$17.8M
Studies of Autism and Related DisordersZ01MH002868 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI SWEDO, SUSAN E. · 2006 to 2008
$4.1M
Mechanisms of Pain and Immune ProcessesZ01DE000724 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI IADAROLA, MICHAEL J. · 2008 to 2008
$848k
Mechanisms of Pain and Immune ProcessesZIACL090034 · CLC · CLINICAL CENTER · PI MANNES, ANDREW · 2014 to 2025
$0k
Intramural NIH HHS Z01 DE000724Intramural NIH HHS Z01 MH002868
6 · The paper itself

Abstract

backgroundThe 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.

methodsSerological 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.

resultsThe 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.

conclusionUsing 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. GENERAL SIGNIFICANCE: The idea that autoantibodies represent an underlying cause or are biomarkers for autism pathophysiology is not supported by this report.

Identifiers

PMID26366376
PMCPMC4564997
OpenAlexW1140638874

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.