Evidence map›Paper›PMID 24439555›Full record

ReviewBiological psychiatry2014

The cytokine model of schizophrenia: emerging therapeutic strategies.

Ragy R Girgis, Samhita S Kumar, Alan S Brown

Abstract readReview
In one paragraph

Review in Biological psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 5 pooled it
3.8field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 5 syntheses or guidelines pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Acetylsalicylic acid (aspirin) for schizophrenia.The Cochrane database of systematic reviews · 2019
    Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Article
  9. Autoimmune neuropsychiatric disorders manifesting with psychosis.The Journal of clinical investigation · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Identification of Factors to Predict Transition to Schizophrenia in Subjects with Ultra-high Risk for Psychosis: A Protocol for a Multicenter, Longitudinal Study of Sleep Parameters and Cytokine Levels.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Maternal Immune Activation Induces Cortical Catecholaminergic Hypofunction and Cognitive Impairments in Offspring.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Article
  18. Review
  19. Article
  20. Review

1 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

3 authors at 3 institutions in 1 country.

Ragy R Girgis *Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Samhita S Kumar *New York State Psychiatric Institute, New York, NY, USA.
Alan S BrownDepartment of Psychiatry, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Columbia University · USNew York Psychoanalytic Society and Institute · USNew York State Psychiatric Institute

Funding

CTSA: K12 COMPONENTKL2RR024157 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2006 to 2011
$8.9M
Epidemiology of Prenatal Factors and Adult PsychopathologyK02MH065422 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BROWN, ALAN STEWART · 2003 to 2012
$1.2M
NCRR NIH HHS 2KL2RR024157-06NCRR NIH HHS KL2 RR024157NIMH NIH HHS 5K02 MH065422NIMH NIH HHS K02 MH065422
6 · The paper itself

Abstract

We discuss the rationale for a trial of a novel biological immunotherapy in schizophrenia (SCZ). Available antipsychotic treatments for SCZ are often limited by partial effectiveness and significant side effects. The search for novel medications is of high priority. All current antipsychotics function primarily by blocking D2-type dopamine receptors. An emerging theory of SCZ postulates disturbances of cytokines and inflammatory mediators (i.e., the cytokine model), possibly originating in part from infectious exposures. Cytokines are one of the most important components of the immune system that orchestrate the response to infectious and other exogenous insults. Preclinical models of SCZ support a convergence between a role for certain cytokines in the pathophysiology of SCZ and major neurochemical postulates of the disorder, including the dopamine and glutamate hypotheses. Several cytokines are elevated in plasma in SCZ, and positron emission tomography studies have shown active inflammation in the brains of patients with psychosis. Treatment studies of anti-inflammatory agents, such as celecoxib and aspirin, in patients with SCZ have provided further support for neuroinflammation in this disorder. The development of approved biological therapies for autoimmune diseases provides new opportunities to target cytokine signaling directly as a novel treatment strategy in SCZ. In addition, advances in imaging, immunology, and psychopharmacology have paved the way for using measures of target engagement of neuroimmune components that would facilitate the identification of patient subgroups who are most likely to benefit from cytokine modulation.

Indexed as

AnimalsAntipsychotic AgentsBrainCytokinesDopamineGlutamic AcidHumansNeuroimmunomodulationSchizophreniaAntipsychotic AgentsCytokinesDopamineGlutamic AcidCytokineinflammationinterleukinmicrobialneuroimmuneschizophrenia

Identifiers

PMID24439555
PMCPMC3931550
OpenAlexW2022949524

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.