Evidence map›Paper›PMID 25540679›Full record

ArticleMolecular autism2014

Association study between autistic-like traits and polymorphisms in the autism candidate regions RELN, CNTNAP2, SHANK3, and CDH9/10.

Lina Jonsson, Anna Zettergren, Erik Pettersson, Daniel Hovey, Henrik Anckarsäter, Lars Westberg, Paul Lichtenstein, Sebastian Lundström, Jonas Melke

Open access · goldAbstract read
In one paragraph

Article in Molecular autism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Association between Genetic Variants inBehavioural neurology · 2021
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  13. 5p deletions: Current knowledge and future directions.American journal of medical genetics. Part C, Seminars in medical genetics · 2015
    Review
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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

9 authors at 3 institutions in 1 country.

Lina JonssonDepartment of Pharmacology, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, POB 431, SE 405 30 Gothenburg, Sweden.
Anna ZettergrenDepartment of Pharmacology, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, POB 431, SE 405 30 Gothenburg, Sweden.
Erik PetterssonDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Daniel HoveyDepartment of Pharmacology, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, POB 431, SE 405 30 Gothenburg, Sweden.
Henrik AnckarsäterDepartment of Forensic Psychiatry, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Lars WestbergDepartment of Pharmacology, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, POB 431, SE 405 30 Gothenburg, Sweden.
Paul LichtensteinDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Sebastian LundströmDepartment of Forensic Psychiatry, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden ; Swedish Prison and probation service, R&D unit, Gothenburg, Sweden ; Gillberg Neuropsychiatry Centre, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Jonas MelkeDepartment of Pharmacology, Institute of Neuroscience and Physiology at the Sahlgrenska Academy, University of Gothenburg, POB 431, SE 405 30 Gothenburg, Sweden.
University of Gothenburg · SEKarolinska Institutet · SESwedish Prison and Probation Service · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutistic-like traits (ALTs) are continuously distributed in the general population, with the autism spectrum disorder (ASD) at the upper extreme end. A genetic overlap has been shown between ALTs and ASD, indicating that common variation in ASD candidate genes may also influence ALTs. In our study, we have investigated the SNP rs4307059 that has been associated with both ALTs and ASD. In addition, we genotyped polymorphisms in a selection of genes involved in synaptic functioning, that is, SHANK3, RELN, and CNTNAP2, which repeatedly have been associated with ASD. The possible associations of these polymorphisms with ALTs, as well as genetic factors for neurodevelopmental problems (NDPs), were investigated in a large cohort from the general population: The Child and Adolescent Twin Study in Sweden. For analyses of ALTs and NDPs, 12,319 subjects (including 2,268 monozygotic (MZ) and 3,805 dizygotic (DZ) twin pairs) and 8,671 subjects (including 2,243 MZ and 2,044 DZ twin pairs), respectively, were included in the analyses.

findingsWe could not replicate the previous association between rs4307059 and social communication impairment. Moreover, common variations in CNTNAP2 (rs7794745 and rs2710102), RELN (rs362691), and SHANK3 (rs9616915) were not significantly associated with ALTs in our study.

conclusionsOur results do not suggest that the investigated genes, which previously has been found associated with ASD diagnosis, have any major influence on ALTs in children from the general population.

Indexed as

A-TACAutism spectrum disorderAutistic-like traitsCATSSCNTNAP2RELNrs4307059SHANK3

Identifiers

PMID25540679
PMCPMC4276093
OpenAlexW2104915321

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.