Evidence map›Paper›PMID 21521612›Full record

ArticleNeuron2011

The neuronal transporter gene SLC6A15 confers risk to major depression.

Martin A Kohli, Susanne Lucae, Philipp G Saemann, Mathias V Schmidt, Ayse Demirkan, Karin Hek, Darina Czamara, Michael Alexander, Daria Salyakina, Stephan Ripke and 29 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 16 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 16 pooled it
14.7field-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

100 citing papers in PubMed, 16 syntheses or guidelines pooled it, 227 citations in OpenAlex.

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  5. The Gene Encoding Protocadherin 9 (PCDH9), a Novel Risk Factor for Major Depressive Disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
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  11. Association of HTR2A T102C and A-1438G polymorphisms with susceptibility to major depressive disorder: a meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
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40 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

39 authors at 9 institutions in 4 countries.

Martin A KohliMax Planck Institute of Psychiatry, D-80804 Munich, Germany.
Susanne Lucae
Philipp G Saemann
Mathias V Schmidt
Ayse Demirkan
Karin Hek
Darina Czamara
Michael Alexander
Daria Salyakina
Stephan Ripke
David Hoehn
Michael Specht
Andreas Menke
Johannes Hennings
Angela Heck
Christiane Wolf
Marcus Ising
Stefan Schreiber
Michael Czisch
Marianne B Müller
Manfred Uhr
Thomas Bettecken
Albert Becker
Johannes Schramm
Marcella Rietschel
Wolfgang Maier
Bekh Bradley
Kerry J Ressler
Markus M Nöthen
Sven Cichon
Ian W Craig
Gerome Breen
Cathryn M Lewis
Albert Hofman
Henning Tiemeier
Cornelia M van Duijn
Florian Holsboer
Bertram Müller-Myhsok
Elisabeth B Binder
Max Planck Institute of Psychiatry · DEErasmus MC · NLUniversity of Bonn · DEKing's College London · GBEmory University · USChristian-Albrechts-Universität zu Kiel · DEHeidelberg University · DEHoward Hughes Medical Institute · USUniversity Hospital Bonn · DE

Funding

Genetic and Trauma-Related Risk Factors for PTSDR01MH071537 · NIMH · EMORY UNIVERSITY · PI RESSLER, KERRY J. · 2005 to 2014
$8.5M
Howard Hughes Medical InstituteMedical Research Council G0701003Medical Research Council G0701420NIMH NIH HHS R01 MH071537Wellcome TrustWellcome Trust 085475
6 · The paper itself

Abstract

Major depression (MD) is one of the most prevalent psychiatric disorders and a leading cause of loss in work productivity. A combination of genetic and environmental risk factors probably contributes to MD. We present data from a genome-wide association study revealing a neuron-specific neutral amino acid transporter (SLC6A15) as a susceptibility gene for MD. Risk allele carrier status in humans and chronic stress in mice were associated with a downregulation of the expression of this gene in the hippocampus, a brain region implicated in the pathophysiology of MD. The same polymorphisms also showed associations with alterations in hippocampal volume and neuronal integrity. Thus, decreased SLC6A15 expression, due to genetic or environmental factors, might alter neuronal circuits related to the susceptibility for MD. Our convergent data from human genetics, expression studies, brain imaging, and animal models suggest a pathophysiological mechanism for MD that may be accessible to drug targeting.

Indexed as

Genetic Predisposition to DiseaseAdultAmino Acid Transport Systems, NeutralAnalysis of VarianceAnimalsAspartic AcidChromosomes, Human, Pair 12Disease Models, AnimalFemaleGene Expression RegulationGene FrequencyGenome-Wide Association StudyGenotypeGermanyHippocampusHumansAmino Acid Transport Systems, NeutralAspartic AcidN-acetylaspartateNerve Tissue ProteinsRNA, MessengerSLC6A15 protein, humanTritium

Identifiers

PMID21521612
PMCPMC3112053
OpenAlexW2003551015

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.