Evidence map›Paper›PMID 21078308›Full record

ReviewBrain research2011

Do common variants play a role in risk for autism? Evidence and theoretical musings.

Bernie Devlin, Nadine Melhem, Kathryn Roeder

Abstract readReview
In one paragraph

Review in Brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

47 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Causal inference in genetic trio studies.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  7. Article
  8. The Drosophila GeneFrontiers in genetics · 2019
    Article
  9. Article
  10. Review
  11. Dopaminergic variants in siblings at high risk for autism: Associations with initiating joint attention.Autism research : official journal of the International Society for Autism Research · 2016
    Article
  12. Recent advances in the genetics of autism spectrum disorder.Current neurology and neuroscience reports · 2015
    Review
  13. Article
  14. Autism spectrum disorders: from genes to neurobiology.Current opinion in neurobiology · 2015
    Review
  15. Review
  16. Autism spectrum disorder: underlying neurobiology.Journal of neural transmission (Vienna, Austria : 1996) · 2014
    Article
  17. Review
  18. Review
  19. Article
  20. Review
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

3 authors.

Bernie DevlinDepartment of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. devlinbj@upmc.edu
Nadine Melhem
Kathryn Roeder

Funding

Genetics Association in Schizophrenia and Other DisordersR37MH057881 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEVLIN, BERNIE · 2013 to 2022
$5.4M
GENETIC ASSOCIATION IN SCHIZOPHRENIA AND OTHER DISORDERSR01MH057881 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEVLIN, BERNIE · 1998 to 2012
$4.8M
Genetic Linkage Study of Depression and Anxiety Disorders in an Arab KindredK01MH077930 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MELHEM, NADINE M. · 2007 to 2011
$755k
Autism Speaks AS7462NIMH NIH HHS K01 MH077930NIMH NIH HHS MH057881NIMH NIH HHS MH077930NIMH NIH HHS R01 MH057881NIMH NIH HHS R37 MH057881
6 · The paper itself

Abstract

Both rare and common genetic variants underlie risk for almost any complex disease. Over the past few years a common tool for identifying common risk variants is genome-wide association or GWA. Our analyses focus on results from GWA targeting common variants affecting risk for autism spectrum disorders (ASD). Thus far three large GWA studies have been published, each of which highlights a single, non-overlapping risk locus. Evaluation of these studies suggests that combination of their data would diminish evidence for all of these loci, making none of them significant. Despite this paucity of findings, statistical theory can be used to infer a plausible distribution of effect sizes for SNPs affecting risk for ASD. We lay out this theory, calculate plausible distributions, and discuss the results in the context of results from GWA studies for schizophrenia.

Indexed as

ChildChild Development Disorders, PervasiveChild, PreschoolGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansInfantPolymorphism, Genetic

Identifiers

PMID21078308
PMCPMC3638767

What OpenQuestion holds

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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.