Evidence map›Paper›PMID 26028548›Full record

ReviewJournal of psychiatric research2015

Kynurenine pathway dysfunction in the pathophysiology and treatment of depression: Evidences from animal and human studies.

Gislaine Z Réus, Karen Jansen, Stephanie Titus, André F Carvalho, Vilma Gabbay, João Quevedo

Open access · greenAbstract readReview
In one paragraph

Review in Journal of psychiatric research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 3 pooled it
5.3field-weighted citation impact, top 3% 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

108 citing papers in PubMed, 3 syntheses or guidelines pooled it, 219 citations in OpenAlex.

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48 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 2 countries.

Gislaine Z RéusCenter for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Medical School at Houston, Houston, TX, USA; Laboratory of Neurosciences, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil. Electronic address: gislaine.z.reus@uth.tmc.edu.
Karen JansenCenter for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Medical School at Houston, Houston, TX, USA; Graduate Program in Health and Behavior, Catholic University of Pelotas, Pelotas, RS, Brazil.
Stephanie TitusCenter for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Medical School at Houston, Houston, TX, USA.
André F CarvalhoDepartment of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.
Vilma GabbayDepartment of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
João QuevedoCenter for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Medical School at Houston, Houston, TX, USA; Laboratory of Neurosciences, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil.
Universidade do Sul de Santa Catarina · BRIcahn School of Medicine at Mount Sinai · USUniversidade Católica de Pelotas · BRUniversidade Federal do Ceará · BR

Funding

Neuroinflammation and PVS Deficits in AdolescentsR01MH101479 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GABBAY, VILMA · 2014 to 2018
$3.1M
The Neuroimmunology of AnhedoniaR01MH095807 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GABBAY, VILMA · 2012 to 2016
$3.0M
NIMH NIH HHS R01 MH095807NIMH NIH HHS R01 MH101479
6 · The paper itself

Abstract

Treatment-resistant depression affects up to 20% of individuals suffering from major depressive disorder (MDD). The medications currently available to treat depression, including serotonin re-uptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs), fail to produce adequate remission of depressive symptoms for a large number of patients. The monoamine hypothesis upon which these medications are predicated should be expanded and revised as research elucidates alternative mechanisms of depression and effective methods to treat the underlying pathologic consequences. Research into the role of tryptophan degradation and the kynurenine pathway in the setting of inflammation has brought new insight into potential etiologies of MDD. Further investigation into the connection between inflammatory mediators, tryptophan degradation, and MDD can provide many targets for novel antidepressant therapies. Thus, this review will highlight the role of the kynurenine pathway in the pathophysiology of depression, as well as a novel therapeutic target to classic and new modulators to treat depression based on findings from preclinical and clinical studies.

Indexed as

AnimalsHumansKynurenineMajor Depressive DisorderMetabolic Networks and PathwaysKynurenineDepressionIndoleamine 2,3–dioxygenaseInflammationKynurenine pathwayTryptophan

Identifiers

PMID26028548
PMCPMC4955923
OpenAlexW1484783577

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.