Evidence map›Paper›PMID 26188008›Full record

ReviewHuman molecular genetics2015

Genetics and genomics of autism spectrum disorder: embracing complexity.

Silvia De Rubeis, Joseph D Buxbaum

Abstract readReview
In one paragraph

Review in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 5 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

110 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Potential of Salivary Biomarkers in Autism Research: A Systematic Review.International journal of molecular sciences · 2021
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Arbaclofen in Children and Adolescents with Autism Spectrum Disorder: A Randomized, Controlled, Phase 2 Trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Trial
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Behavioral decline in Shank3Molecular autism · 2024
    Article
  20. Article

50 more citing papers are in PubMed but not listed here.

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

2 authors.

Silvia De RubeisSeaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA Department of Psychiatry, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA.
Joseph D BuxbaumSeaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA Department of Psychiatry, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA Department of Neuroscience, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA and The Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA joseph.buxbaum@mssm.edu.

Funding

1/4-The Autism Sequencing Consortium: Autism gene discovery in >20,000 exomesU01MH100233 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BUXBAUM, JOSEPH D. · 2013 to 2015
$2.5M
NIMH NIH HHS U01MH100233
6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder (NDD) characterized by impairments in social communication and social interaction and the presence of repetitive behaviors and/or restricted interests. ASD has profound etiological and clinical heterogeneity, which has impeded the identification of risk factors and pathophysiological processes underlying the disorder. A constellation of (i) types of genetic variation, (ii) modes of inheritance and (iii) specific genomic loci and genes have all recently been implicated in ASD risk, and these findings are currently being extended with functional analyses in model organisms and genotype-phenotype correlation studies. The overlap of risk loci between ASD and other NDDs raises intriguing questions around the mechanisms of risk. In this review, we will touch upon these aspects of ASD and how they might be addressed.

Indexed as

GenomicsAnimalsAutism Spectrum DisorderGenetic Association StudiesGenetic VariationHumansInheritance PatternsRisk Factors

Identifiers

PMID26188008
PMCPMC4675826

What OpenQuestion holds

Textmetadata
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.