Evidence map›Paper›PMID 28653857›Full record

ReviewJournal of psychopharmacology (Oxford, England)2017

Anti-inflammatory treatment for major depressive disorder: implications for patients with an elevated immune profile and non-responders to standard antidepressant therapy.

Paula Kopschina Feltes, Janine Doorduin, Hans C Klein, Luis Eduardo Juárez-Orozco, Rudi Ajo Dierckx, Cristina M Moriguchi-Jeckel, Erik Fj de Vries

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of psychopharmacology (Oxford, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 2% 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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 272 citations in OpenAlex.

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  11. Inflammatory Biomarkers in Acute Suicidal Behaviors.International journal of molecular sciences · 2026
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54 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

7 authors at 2 institutions in 2 countries.

Paula Kopschina Feltes1 Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, Groningen, the Netherlands.
Janine Doorduin1 Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, Groningen, the Netherlands.
Hans C Klein1 Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, Groningen, the Netherlands.
Luis Eduardo Juárez-Orozco1 Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, Groningen, the Netherlands.
Rudi Ajo Dierckx1 Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, Groningen, the Netherlands.
Cristina M Moriguchi-Jeckel2 Instituto de Geriatria e Gerontologia, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brasil.
Erik Fj de Vries1 Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, Groningen, the Netherlands.
University Medical Center Groningen · NLInstituto do Cérebro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major depressive disorder (MDD) is a prevalent and disabling psychiatric disease with rates of non-responsiveness to antidepressants ranging from 30-50%. Historically, the monoamine depletion hypothesis has dominated the view on the pathophysiology of depression. However, the lack of responsiveness to antidepressants and treatment resistance suggests that additional mechanisms might play a role. Evidence has shown that a subgroup of depressive patients may have an underlying immune deregulation that could explain the lack of therapeutic benefit from antidepressants. Stimuli like inflammation and infection can trigger the activation of microglia to release pro-inflammatory cytokines, acting on two main pathways: (1) activation of the hypothalamic-pituitary adrenal axis, generating an imbalance in the serotonergic and noradrenergic circuits; (2) increased activity of the enzyme indoleamine-2,3-dioxygenase, resulting in depletion of serotonin levels and the production of quinolinic acid. If this hypothesis is proven true, the subgroup of MDD patients with increased levels of pro-inflammatory cytokines, mainly IL-6, TNF-α and IL-1β, might benefit from an anti-inflammatory intervention. Here, we discuss the pre-clinical and clinical studies that have provided support for treatment with non-steroidal anti-inflammatory drugs in depressed patients with inflammatory comorbidities or an elevated immune profile, as well as evidences for anti-inflammatory properties of standard antidepressants.

Indexed as

Antidepressive AgentsAnti-Inflammatory AgentsHumansHypothalamo-Hypophyseal SystemInflammationMajor Depressive DisorderPituitary-Adrenal SystemSerotoninAntidepressive AgentsAnti-Inflammatory AgentsSerotoninantidepressantsMajor depressive disordermicroglianeuroinflammationpro-inflammatory cytokines

Identifiers

PMID28653857
PMCPMC5606303
OpenAlexW2730275538

What OpenQuestion holds

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LicenceCC BY-NC
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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.