Evidence map›Paper›PMID 25850031›Full record

Trial reportThe pharmacogenomics journal2015

Neuronal cell adhesion genes and antidepressant response in three independent samples.

C Fabbri, C Crisafulli, D Gurwitz, J Stingl, R Calati, D Albani, G Forloni, M Calabrò, R Martines, S Kasper and 7 more

Abstract readClinical TrialMulticenter Study
PubMed Publisher
In one paragraph

Trial report in The pharmacogenomics journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 3 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. The expressions and mFrontiers in genetics · 2026
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  17. The Genetics of Treatment-Resistant Depression: A Critical Review and Future Perspectives.The international journal of neuropsychopharmacology · 2019
    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

17 authors at 8 institutions in 5 countries.

C FabbriDepartment of Biomedical and NeuroMotor Sciences, University of Bologna, Bologna, Italy.
C CrisafulliDepartment of Biomedical Science and Morphological and Functional Images, University of Messina, Messina, Italy.
D GurwitzDepartment of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Italy.
J StinglFederal Institute for Drugs and Medical Devices, University Bonn Medical School, Bonn, Germany.
R CalatiFaculty Centre for Translational Medicine, University Bonn, Medical Faculty, Bonn, Germany.
D AlbaniLaboratory of Biology of Neurodegenerative Disorders, Department of Neuroscience, IRCCS Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy.ORCID http://orcid.org/0000-0002-7050-6723
G ForloniLaboratory of Biology of Neurodegenerative Disorders, Department of Neuroscience, IRCCS Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy.
M CalabròDepartment of Biomedical Science and Morphological and Functional Images, University of Messina, Messina, Italy.
R MartinesDepartment of Biomedical and NeuroMotor Sciences, University of Bologna, Bologna, Italy.
S KasperDepartment of Psychiatry and Psychotherapy, Medical University Vienna, Vienna, Austria.
J ZoharDepartment of Psychiatry, Sheba Medical Center, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
A Juven-WetzlerDepartment of Psychiatry, Sheba Medical Center, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
D SoueryLaboratoire de Psychologie Medicale, Universitè Libre de Bruxelles and Psy Pluriel, Centre Européen de Psychologie Medicale, Brussels, Belgium.
S Montgomerylmperial College School of Medicine, London, UK.
J MendlewiczUniversité Libre de Bruxelles, Brussels, Belgium.
G D GirolamoFaculty Centre for Translational Medicine, University Bonn, Medical Faculty, Bonn, Germany.
A SerrettiDepartment of Biomedical and NeuroMotor Sciences, University of Bologna, Bologna, Italy.
Mario Negri Institute for Pharmacological Research · ITTel Aviv University · ILUniversité Libre de Bruxelles · BEUniversity of Bologna · ITUniversity of Bonn · DEUniversity of Messina · ITFederal Institute for Drugs and Medical Devices · DEMedical University of Vienna · AT

Funding

TREATMENT RESISTANT DEPRESSIONN01MH90003 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · 2007 to 2008
$9.1M
TREATMENT RESISTANT DEPRESSION-278990003N01MH090003 · NIMH · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · 1999 to 2003
–
NIMH NIH HHS N01MH90003
6 · The paper itself

Abstract

Drug-effect phenotypes in human lymphoblastoid cell lines recently allowed to identify CHL1 (cell adhesion molecule with homology to L1CAM), GAP43 (growth-associated protein 43) and ITGB3 (integrin beta 3) as new candidates for involvement in the antidepressant effect. CHL1 and ITGB3 code for adhesion molecules, while GAP43 codes for a neuron-specific cytosolic protein expressed in neuronal growth cones; all the three gene products are involved in synaptic plasticity. Sixteen polymorphisms in these genes were genotyped in two samples (n=369 and 90) with diagnosis of major depressive episode who were treated with antidepressants in a naturalistic setting. Phenotypes were response, remission and treatment-resistant depression. Logistic regression including appropriate covariates was performed. Genes associated with outcomes were investigated in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) genome-wide study (n=1861) as both individual genes and through a pathway analysis (Reactome and String databases). Gene-based analysis suggested CHL1 rs4003413, GAP43 rs283393 and rs9860828, ITGB3 rs3809865 as the top candidates due to their replication across the largest original sample and the STAR*D cohort. GAP43 molecular pathway was associated with both response and remission in the STAR*D, with ELAVL4 representing the gene with the highest percentage of single nucleotide polymorphisms (SNPs) associated with outcomes. Other promising genes emerging from the pathway analysis were ITGB1 and NRP1. The present study was the first to analyze cell adhesion genes and their molecular pathways in antidepressant response. Genes and biomarkers involved in neuronal adhesion should be considered by further studies aimed to identify predictors of antidepressant response.

Indexed as

Antidepressive AgentsBiomarkersCell AdhesionCell Adhesion MoleculesCell Adhesion Molecules, NeuronalFemaleGAP-43 ProteinGenome-Wide Association StudyGenotypeHumansIntegrin beta3Major Depressive DisorderMaleMiddle AgedPolymorphism, Single NucleotideAntidepressive AgentsBiomarkersCell Adhesion MoleculesCell Adhesion Molecules, NeuronalCHL1 protein, humanGAP-43 ProteinIntegrin beta3ITGB3 protein, human

Identifiers

PMID25850031
OpenAlexW1966688595

What OpenQuestion holds

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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.