Evidence mapPaperPMID 28847294Full record

ReviewCurrent neuropharmacology2018

Therapeutic Strategies for Treatment of Inflammation-related Depression.

Miroslav Adzic, Zeljka Brkic, Milos Mitic, Ester Francija, Milica J Jovicic, Jelena Radulovic, Nadja P Maric

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 4 pooled it
3.1field-weighted citation impact, top 8% 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

70 citing papers in PubMed, 4 syntheses or guidelines pooled it, 164 citations in OpenAlex.

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  5. Trial
  6. Psychological Distress, Resilience, and Immunoinflammatory Signatures in Healthcare Workers During COVID-19.Stress and health : journal of the International Society for the Investigation of Stress · 2026
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10 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 3 institutions in 2 countries.

Miroslav AdzicDepartment of Molecular Biology and Endocrinology, VINCA Institute of Nuclear Sciences, University of Belgrade, Serbia.
Zeljka BrkicDepartment of Molecular Biology and Endocrinology, VINCA Institute of Nuclear Sciences, University of Belgrade, Serbia.
Milos MiticDepartment of Molecular Biology and Endocrinology, VINCA Institute of Nuclear Sciences, University of Belgrade, Serbia.
Ester FrancijaDepartment of Molecular Biology and Endocrinology, VINCA Institute of Nuclear Sciences, University of Belgrade, Serbia.
Milica J JovicicClinic for Psychiatry, Clinical Centre of Serbia, Pasterova 2, 11000, Belgrade, Serbia.
Jelena RadulovicDepartment of Psychiatry and Behavioral Sciences, The Asher Center of Study and Treatment of Depressive Disorders, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.
Nadja P MaricClinic for Psychiatry, Clinical Centre of Serbia, Pasterova 2, 11000, Belgrade, Serbia.
University of Belgrade · RSCentar za Promociju Nauke · RSNorthwestern University · US

Funding

NIMH NIH HHS R21 MH098793
6 · The paper itself

Abstract

backgroundMounting evidence demonstrates enhanced systemic levels of inflammatory mediators in depression, indicating that inflammation may play a role in the etiology and course of mood disorders. Indeed, proinflammatory cytokines induce a behavioral state of conservation- withdrawal resembling human depression, characterized by negative mood, fatigue, anhedonia, psychomotor retardation, loss of appetite, and cognitive deficits. Neuroinflammation also contributes to non-responsiveness to current antidepressant (AD) therapies. Namely, response to conventional AD medications is associated with a decrease in inflammatory biomarkers, whereas resistance to treatment is accompanied by increased inflammation.

methodsIn this review, we will discuss the utility and shortcomings of pharmacologic AD treatment strategies focused on inflammatory pathways, applied alone or as an adjuvant component to current AD therapies.

resultsMechanisms of cytokine actions on behavior involve activation of inflammatory pathways in the brain, resulting in changes of neurotransmitter metabolism, neuroendocrine function, and neuronal plasticity. Selective serotonin reuptake inhibitors exhibit the most beneficial effects in restraining the inflammation markers in depression. Different anti-inflammatory agents exhibit AD effects via modulating neurotransmitter systems, neuroplasticity markers and glucocorticoid receptor signaling. Anti-inflammatory add-on therapy in depression highlights such treatment as a candidate for enhancement strategy in patients with moderate-to-severe depression.

conclusionThe interactions between the immune system and CNS are not only involved in shaping behavior, but also in responding to therapeutics. Even though, substantial evidence from animal and human research support a beneficial effect of anti-inflammatory add-on therapy in depression, further research with special attention on safety, particularly during prolonged periods of antiinflammatory co-treatments, is required.

Indexed as

AnimalsAntidepressive AgentsAnti-Inflammatory AgentsBrainCytokininsDepressionHumansInflammationAntidepressive AgentsAnti-Inflammatory AgentsCytokininsantidepressantsanti-inflammatory drugsDepressioninflammationside effectstreatment

Identifiers

PMID28847294
PMCPMC5883379
OpenAlexW2753851455

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.