Evidence map›Paper›PMID 25483344›Full record

ReviewBiological psychiatry2015

Genetic epidemiology and insights into interactive genetic and environmental effects in autism spectrum disorders.

Young Shin Kim, Bennett L Leventhal

Open access · greenAbstract readReview
In one paragraph

Review in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 5 pooled it
9.1field-weighted citation impact, top 1% 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

123 citing papers in PubMed, 5 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

63 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 at 2 institutions in 2 countries.

Young Shin KimDepartment of Psychiatry, University of California, San Francisco, San Francisco, California.. Electronic address: youngshin.kim@ucsf.edu.
Bennett L LeventhalDepartment of Psychiatry, Yonsei University College of Medicine, Seoul, South Korea.
University of California, San Francisco · USYonsei University · KR

Funding

The Roles of Environmental Risks and GEX in Increasing ASD PrevalenceR01ES021462 · NIEHS · YALE UNIVERSITY · PI KIM, YOUNG SHIN · 2012 to 2018
$4.1M
NIEHS NIH HHS R01 ES021462NIEHS NIH HHS R01ES021462
6 · The paper itself

Abstract

Understanding the pathogenesis of neurodevelopmental disorders has proven to be challenging. Using autism spectrum disorder (ASD) as a paradigmatic neurodevelopmental disorder, this article reviews the existing literature on the etiological substrates of ASD and explores how genetic epidemiology approaches including gene-environment interactions (G×E) can play a role in identifying factors associated with ASD etiology. New genetic and bioinformatics strategies have yielded important clues to ASD genetic substrates. The next steps for understanding ASD pathogenesis require significant effort to focus on how genes and environment interact with one another in typical development and its perturbations. Along with larger sample sizes, future study designs should include sample ascertainment that is epidemiologic and population-based to capture the entire ASD spectrum with both categorical and dimensional phenotypic characterization; environmental measurements with accuracy, validity, and biomarkers; statistical methods to address population stratification, multiple comparisons, and G×E of rare variants; animal models to test hypotheses; and new methods to broaden the capacity to search for G×E, including genome-wide and environment-wide association studies, precise estimation of heritability using dense genetic markers, and consideration of G×E both as the disease cause and a disease course modifier. Although examination of G×E appears to be a daunting task, tremendous recent progress in gene discovery has opened new horizons for advancing our understanding of the role of G×E in the pathogenesis of ASD and ultimately identifying the causes, treatments, and even preventive measures for ASD and other neurodevelopmental disorders.

Indexed as

Gene-Environment InteractionChild Development Disorders, PervasiveHumansMolecular EpidemiologyTwin Studies as TopicAutism spectrum disordersEnvironmentGenesGenetic epidemiologyInteractionsNeurodevelopmental disorders

Identifiers

PMID25483344
PMCPMC4260177
OpenAlexW2010765482

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.