Evidence map›Paper›PMID 23644052›Full record

ReviewNeuroscience2013

Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications.

J C Felger, F E Lotrich

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02628054 (Investigating the Effects of Typhoid Vaccine on Sleep in Healthy Volunteers), which is not on this map. Cited by 542 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
542citing papers in PubMed, 10 pooled it
14.5field-weighted citation impact, top 1% 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.

NCT02628054 nacompletednot on this mapstarted 2015, after this paper: background citation

Investigating the Effects of Typhoid Vaccine on Sleep in Healthy Volunteers

TypeinterventionalSponsorUniversity of OxfordRan2015 to 2015Enrolled16ConditionsTyphoid Vaccine on SleepArmsTyphoid Vaccine, Placebo
3 · Its place in the literature

Who cites it

542 citing papers in PubMed, 10 syntheses or guidelines pooled it, 1,128 citations in OpenAlex.

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482 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

2 authors at 2 institutions in 1 country.

J C FelgerDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30306, United States. jfelger@gmail.com
F E Lotrich
Emory University · USUniversity of Pittsburgh · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
RESEARCH METHODS COREP30MH090333 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REYNOLDS, CHARLES F. · 2011 to 2015
$8.3M
Vulnerability to major depression: The role of delta sleep in patients receivingR01MH090250 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LOTRICH, FRANCIS E · 2010 to 2014
$1.6M
NCATS NIH HHS UL1 TR000005NCI NIH HHS P30 CA138292NIMH NIH HHS P30 MH090333NIMH NIH HHS R01 MH090250PHS HHS R090250
6 · The paper itself

Abstract

Mounting evidence indicates that inflammatory cytokines contribute to the development of depression in both medically ill and medically healthy individuals. Cytokines are important for development and normal brain function, and have the ability to influence neurocircuitry and neurotransmitter systems to produce behavioral alterations. Acutely, inflammatory cytokine administration or activation of the innate immune system produces adaptive behavioral responses that promote conservation of energy to combat infection or recovery from injury. However, chronic exposure to elevated inflammatory cytokines and persistent alterations in neurotransmitter systems can lead to neuropsychiatric disorders and depression. Mechanisms of cytokine behavioral effects involve activation of inflammatory signaling pathways in the brain that results in changes in monoamine, glutamate, and neuropeptide systems, and decreases in growth factors, such as brain-derived neurotrophic factor. Furthermore, inflammatory cytokines may serve as mediators of both environmental (e.g. childhood trauma, obesity, stress, and poor sleep) and genetic (functional gene polymorphisms) factors that contribute to depression's development. This review explores the idea that specific gene polymorphisms and neurotransmitter systems can confer protection from or vulnerability to specific symptom dimensions of cytokine-related depression. Additionally, potential therapeutic strategies that target inflammatory cytokine signaling or the consequences of cytokines on neurotransmitter systems in the brain to prevent or reverse cytokine effects on behavior are discussed.

Indexed as

AnimalsAntidepressive AgentsBiomarkersBrainCytokinesDepressionHumansInflammationInflammation MediatorsAntidepressive AgentsBiomarkersCytokinesInflammation Mediators

Identifiers

PMID23644052
PMCPMC3741070
OpenAlexW2004243143

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.