Evidence map›Paper›PMID 23277131›Full record

ArticlePsychiatric genetics2013

A large-scale candidate gene analysis of mood disorders: evidence of neurotrophic tyrosine kinase receptor and opioid receptor signaling dysfunction.

Anthony J Deo, Yung-yu Huang, Colin A Hodgkinson, Yurong Xin, Maria A Oquendo, Andrew J Dwork, Victoria Arango, David A Brent, David Goldman, J John Mann and 1 more

Abstract read
In one paragraph

Article in Psychiatric genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-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

8 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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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

11 authors at 3 institutions in 1 country.

Anthony J DeoDepartment of Psychiatry, Division of Molecular Imaging and Neuropathology, New York State Psychiatric Institute, Columbia University, New York, NY 10032, USA.
Yung-yu Huang
Colin A Hodgkinson
Yurong Xin
Maria A Oquendo
Andrew J Dwork
Victoria Arango
David A Brent
David Goldman
J John Mann
Fatemeh Haghighi
Columbia University · USNational Institute on Alcohol Abuse and Alcoholism · USNew York Psychoanalytic Society and Institute · US

Funding

Integrative genetics of behavior with high throughput technologiesZIAAA000301 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI GOLDMAN, DAVID · 2009 to 2025
$68.6M
THE NEUROBIOLOGY OF SUICIDAL BEHAVIORP50MH062185 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI MANN, JOSEPH JOHN · 2000 to 2009
$21.7M
POSTMORTEM NEUROCHEMICAL STUDIES IN SUICIDER01MH040210 · NIMH · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI UNDERWOOD, MARK D · 1985 to 2016
$7.0M
Golgi Studies of SchizophreniaR01MH064168 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI DWORK, ANDREW J · 2001 to 2013
$4.3M
PSYCHOBIOLOGICAL PREDICTORS OF SUICIDAL BEHAVIOR IN MDER01MH048514 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OQUENDO, MARIA A · 1992 to 2013
$3.6M
PHARMACOTHERAPY OF HIGH-RISK BIPOLAR DISORDERR01MH059710 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE · PI OQUENDO, MARIA A. · 2000 to 2004
$3.1M
An Integrated Framework of Epigenomics and Human DiseaseR01MH074118 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI HAGHIGHI, FATEMEH G · 2005 to 2009
$2.1M
An Integrated Framework of Epigenomics and Human DiseaseK22HG002915 · NHGRI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HAGHIGHI, FATEMEH G · 2005 to 2009
$1.2M
Gene-Environment Interations Underlying Alcoholism Vulnerability DisordersZIAAA000306 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI GOLDMAN, DAVID · 2009 to 2016
$839k
Gene-Environment Interations Underlying Alcoholism Vulnerability DisordersZ01AA000306 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI GOLDMAN, DAVID · 2006 to 2008
$122k
Intramural NIH HHS Z01 AA000306NHGRI NIH HHS K22 HG002915NHGRI NIH HHS K22 HG2915NIMH NIH HHS MH074118NIMH NIH HHS MH40210NIMH NIH HHS MH48514NIMH NIH HHS MH59710NIMH NIH HHS MH62185NIMH NIH HHS MH64168NIMH NIH HHS P50 MH062185NIMH NIH HHS R01 MH040210NIMH NIH HHS R01 MH048514NIMH NIH HHS R01 MH059710NIMH NIH HHS R01 MH064168NIMH NIH HHS R01 MH074118
6 · The paper itself

Abstract

backgroundDespite proven heritability, little is known about the genetic architecture of mood disorders. Although a number of family and case-control studies have examined the genetics of mood disorders, none have carried out joint linkage-association studies and sought to validate the results with gene expression analyses in an independent cohort.

methodsWe present findings from a large candidate gene study that combines linkage and association analyses using families and singletons, providing a systematic candidate gene investigation of mood disorder. For this study, 876 individuals were recruited, including 83 families with 313 individuals and 563 singletons. This large-scale candidate gene analysis included 130 candidate genes implicated in addictive and other psychiatric disorders. These data showed significant genetic associations for 28 of these candidate genes, although none remained significant after correction for multiple testing. To evaluate the functional significance of these 28 candidate genes in mood disorders, we examined the transcriptional profiles of these genes within the dorsolateral prefrontal cortex and anterior cingulate for 21 cases with mood disorders and 25 nonpsychiatric controls, and carried out a pathway analysis to identify points of high connectivity suggestive of particular molecular pathways that may be dysregulated.

resultsTwo primary gene candidates were supported by the linkage-association, gene expression profiling, and network analysis: neurotrophic tyrosine kinase receptor, type 2 (NTRK2), and the opioid receptor, κ1 (OPRK1).

conclusionThis study supports a role for NTRK2 and OPRK1 signaling in the pathophysiology of mood disorder. The unique approach incorporating evidence from multiple experimental and computational modalities enhances confidence in these findings.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseAdultFemaleGene Expression ProfilingGene Regulatory NetworksGenes, RecessiveHumansMaleModels, GeneticMood DisordersReceptors, Opioid, kappaReceptor, trkBSignal TransductionOPRK1 protein, humanReceptors, Opioid, kappaReceptor, trkB

Identifiers

PMID23277131
PMCPMC3869619
OpenAlexW2082591806

What OpenQuestion holds

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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.