Evidence map›Paper›PMID 25408912›Full record

ArticleJournal of molecular psychiatry2014

Association study in siblings and case-controls of serotonin- and oxytocin-related genes with high functioning autism.

Johanna Nyffeler, Susanne Walitza, Elise Bobrowski, Ronnie Gundelfinger, Edna Grünblatt

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
3.0field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it, 41 citations in OpenAlex.

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  17. Autism-Like Behavior in BTBR Mice Is Improved by Electroconvulsive Therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
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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

5 authors at 2 institutions in 2 countries.

Johanna NyffelerUniversity Clinics of Child and Adolescent Psychiatry (UCCAP), University of Zurich, Thurgauerstr. 39, CH-8050 Zurich, Switzerland.
Susanne WalitzaUniversity Clinics of Child and Adolescent Psychiatry (UCCAP), University of Zurich, Thurgauerstr. 39, CH-8050 Zurich, Switzerland ; Neuroscience Center Zurich, University of Zurich and ETH Zurich, Zurich, Switzerland.
Elise BobrowskiUniversity Clinics of Child and Adolescent Psychiatry (UCCAP), University of Zurich, Thurgauerstr. 39, CH-8050 Zurich, Switzerland ; Department of Experimental Psychology, University of Regensburg, Regensburg, Germany.
Ronnie GundelfingerUniversity Clinics of Child and Adolescent Psychiatry (UCCAP), University of Zurich, Thurgauerstr. 39, CH-8050 Zurich, Switzerland.
Edna GrünblattUniversity Clinics of Child and Adolescent Psychiatry (UCCAP), University of Zurich, Thurgauerstr. 39, CH-8050 Zurich, Switzerland ; Neuroscience Center Zurich, University of Zurich and ETH Zurich, Zurich, Switzerland.
University of Zurich · CHUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism spectrum disorder (ASD) is heritable and neurodevelopmental with unknown causes. The serotonergic and oxytocinergic systems are of interest in autism for several reasons: (i) Both systems are implicated in social behavior, and abnormal levels of serotonin and oxytocin have been found in people with ASD; (ii) treatment with selective serotonin reuptake inhibitors and oxytocin can yield improvements; and (iii) previous association studies have linked the serotonin transporter (SERT; SLC6A4), serotonin receptor 2A (HTR2A), and oxytocin receptor (OXTR) genes with ASD. We examined their association with high functioning autism (HFA) including siblings and their interaction.

methodsIn this association study with HFA children (IQ > 80), siblings, and controls, participants were genotyped for four single nucleotide polymorphisms (SNPs) in OXTR (rs2301261, rs53576, rs2254298, rs2268494) and one in HTR2A (rs6311) as well as the triallelic HTTLPR (SERT polymorphism).

resultsWe identified a nominal significant association with HFA for the HTTLPR s allele (consisting of S and LG alleles) (p = .040; odds ratio (OR) = 1.697, 95% CI 1.191-2.204)). Four polymorphisms (HTTLPR, HTR2A rs6311, OXTR rs2254298 and rs53576) in combination conferred nominal significant risk for HFA with a genetic score of ≥4 (OR = 2.09, 95% CI 1.05-4.18, p = .037). The resulting area under the receiver operating characteristic curve was 0.595 (p = .033).

conclusionsOur findings, combined with those of previous reports, indicate that ASD, in particular HFA, is polygenetic rather than monogenetic and involves the serotonergic and oxytocin pathways, probably in combination with other factors.

Indexed as

Autism spectrum disorderHigh functioning autismOxytocin receptorPolymorphismSerotonin receptor 2ASerotonin transporter

Identifiers

PMID25408912
PMCPMC4223888
OpenAlexW2126119150

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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.