Evidence map›Paper›PMID 23097380›Full record

ArticleAutism research : official journal of the International Society for Autism Research2012

Autism risk gene MET variation and cortical thickness in typically developing children and adolescents.

Alexis Hedrick, Yohan Lee, Gregory L Wallace, Deanna Greenstein, Liv Clasen, Jay N Giedd, Armin Raznahan

Open access · greenAbstract read
In one paragraph

Article in Autism research : official journal of the International Society for Autism Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Differential impact ofNeurobiology of stress · 2018
    Article
  11. Imaging genetics in neurodevelopmental psychopathology.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017
    Review
  12. Review
  13. Article
  14. Article
  15. Insulin-Independent GABAA Receptor-Mediated Response in the Barrel Cortex of Mice with Impaired Met Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Neural signatures of autism spectrum disorders: insights into brain network dynamics.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    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

7 authors at 2 institutions in 1 country.

Alexis HedrickChild Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20814, USA.
Yohan Lee
Gregory L Wallace
Deanna Greenstein
Liv Clasen
Jay N Giedd
Armin Raznahan
National Institutes of Health · USNational Institute of Mental Health · US

Funding

Section on Developmental NeurogenomicsZIAMH002949 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI RAZNAHAN, ARMIN · 2016 to 2025
$30.0M
Intramural NIH HHS Z99 MH999999Medical Research Council G0701370
6 · The paper itself

Abstract

MET receptor tyrosine kinase (MET) has been proposed as a candidate risk gene for autism spectrum disorder (ASD) based on associations between MET polymorphisms and ASD diagnosis, as well as evidence from animal studies that MET protein may regulate early development of cortical regions implicated in the neurobiology of ASD. The relevance of differences in MET signaling for human cortical development remains unexamined, however. We sought to address this issue by relating genotype at a functional single nucleotide polymorphism within the MET promoter (rs1858830, G→C) to in vivo measures of cortical thickness (CT) development derived from 222 healthy children and adolescents with 514 longitudinally acquired structural magnetic resonance imaging brain scans between ages 9 and 22 years. We identified a statistically significant, developmentally fixed, and stepwise CT reduction with increasing C allele dose in superior and middle temporal gyri, ventral precentral and postcentral gyri, and anterior cingulate bilaterally, and in the right frontopolar cortex. We were also able to demonstrate that mean CT within these cortical regions showed a statistically significant reduction with increasing scores on a continuous measure of autistic traits (the Social Responsiveness Scale). The cortical regions highlighted by our analyses are not only established areas of MET expression during prenatal life but are also key components of the "social brain" that have frequently shown structural and functional abnormalities in autism. Our results suggest that genetic differences in the MET gene may influence the development of cortical systems implicated in the neurobiology of ASD.

Indexed as

Child DevelopmentAdolescentAdultAutistic DisorderCerebral CortexChildFemaleGenetic Predisposition to DiseaseHumansImaging, Three-DimensionalLongitudinal StudiesMagnetic Resonance ImagingMalePolymorphism, Single NucleotideProto-Oncogene Proteins c-metYoung AdultMET protein, humanProto-Oncogene Proteins c-met

Identifiers

PMID23097380
PMCPMC3528800
OpenAlexW1796519617

What OpenQuestion 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 OpenQuestion graph.