Evidence map›Paper›PMID 23039393›Full record

ReviewExpert review of neurotherapeutics2012

Elevated immune-inflammatory signaling in mood disorders: a new therapeutic target?

Robert K McNamara, Francis E Lotrich

Open access · greenAbstract readReview
In one paragraph

Review in Expert review of neurotherapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 3 pooled it
3.2field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 3 syntheses or guidelines pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Secondary Mania induced by TNF-α inhibitors: A systematic review.Psychiatry and clinical neurosciences · 2022
    Pooled it
  3. Pooled it
  4. Trial
  5. Choroid plexus inflammation in bipolar disorder.Brain, behavior, and immunity · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Advances and Challenges in Depression Marker Research.Neuropsychiatric disease and treatment · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Circulating JKAP levels may correlate with postpartum anxiety and depression through its interaction with T helper 17 cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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.

Robert K McNamaraDepartment of Psychiatry, Division of Bipolar Disorders Research, University of Cincinnati College of Medicine, Cincinnati, OH, USA. robert.mcnamara@uc.edu
Francis E Lotrich
University of Cincinnati Medical Center · USUniversity of Pittsburgh · US

Funding

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
Omega-3 and Blueberry Supplmentation in Age-Related Cognitive DeclineR01AG034617 · NIA · UNIVERSITY OF CINCINNATI · PI KRIKORIAN, ROBERT · 2009 to 2011
$1.3M
Neurochemical Effects of Omega-3 Fatty Acids in Adolescents at Risk for ManiaR34MH083924 · NIMH · UNIVERSITY OF CINCINNATI · PI DELBELLO, MELISSA P, MCNAMARA, ROBERT K. · 2009 to 2011
$704k
NIA NIH HHS AG03617NIA NIH HHS R01 AG034617NIMH NIH HHS MH083924NIMH NIH HHS MH090250NIMH NIH HHS R01 MH090250NIMH NIH HHS R34 MH083924
6 · The paper itself

Abstract

Converging translational evidence has implicated elevated immune-inflammatory signaling activity in the pathoetiology of mood disorders, including major depressive disorder and bipolar disorder. This is supported in part by cross-sectional evidence for increased levels of proinflammatory eicosanoids, cytokines and acute-phase proteins during mood episodes, and prospective longitudinal evidence for the emergence of mood symptoms in response to chronic immune-inflammatory activation. In addition, mood-stabilizer and atypical antipsychotic medications downregulate initial components of the immune-inflammatory signaling pathway, and adjunctive treatment with anti-inflammatory agents augment the therapeutic efficacy of antidepressant, mood stabilizer and atypical antipsychotic medications. Potential pathogenic mechanisms linked with elevated immune-inflammatory signaling include perturbations in central serotonin neurotransmission and progressive white matter pathology. Both heritable genetic factors and environmental factors including dietary fatty-acid composition may act in concert to sustain elevated immune-inflammatory signaling. Collectively, these data suggest that elevated immune-inflammatory signaling is a mechanism that is relevant to the pathoetiology of mood disorders, and may therefore represent a new therapeutic target for the development of more effective treatments.

Indexed as

Molecular Targeted TherapyAnimalsAnti-Inflammatory Agents, Non-SteroidalAntipsychotic AgentsCytokinesDrug SynergismEvidence-Based MedicineHumansImmune SystemImmunosuppressive AgentsMood DisordersSignal TransductionAnti-Inflammatory Agents, Non-SteroidalAntipsychotic AgentsCytokinesImmunosuppressive Agents

Identifiers

PMID23039393
PMCPMC3535180
OpenAlexW2169473496

What Socratic 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 Socratic graph.