Evidence map›Paper›PMID 27225497›Full record

ReviewCurrent topics in behavioral neurosciences2017

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches.

Robert Dantzer

Open access · greenAbstract readReview
In one paragraph

Review in Current topics in behavioral neurosciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 7 pooled it
8.7field-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.

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

125 citing papers in PubMed, 7 syntheses or guidelines pooled it, 232 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Review
  13. Article
  14. Cross-Organ Neuroimmunology of Behavior.Annual review of immunology · 2026
    Review
  15. Rewiring the Lung-CNS Axis After Spinal Cord Injury.Journal of inflammation research · 2026
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

65 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

1 author at 1 institution in 1 country.

Robert DantzerDepartment of Symptom Research, The University of Texas, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, 77030, USA. rdantzer@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Neuroimmune Mechanisms of Recovery from Comorbid Depression and Chronic PainR01NS073939 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANTZER, ROBERT, HEIJNEN, COBI J · 2011 to 2020
$4.0M
The Metabolic Basis of Cancer-Related FatigueR01CA193522 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANTZER, ROBERT · 2015 to 2023
$3.8M
A novel molecular switch regulating transition from acute to chronic pain.R01NS074999 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KAVELAARS, ANNEMIEKE · 2011 to 2015
$1.7M
Blood-Brain Barrier Transport Mechanisms in Inflammation-Induced DepressionR21MH104694 · NIMH · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANTZER, ROBERT · 2015 to 2016
$444k
Targeting Neural Mitochondria to Treat Chemotherapy-Induced Peripheral NeuropathyR21CA183736 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANTZER, ROBERT, HEIJNEN, COBI J · 2014 to 2015
$383k
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA193522NCI NIH HHS R21 CA183736NIMH NIH HHS R21 MH104694NINDS NIH HHS R01 NS073939NINDS NIH HHS R01 NS074999
6 · The paper itself

Abstract

Physically ill patients with chronic inflammation often present with symptoms of depression. Our understanding of the pathophysiology of inflammation-associated depression has benefited from preclinical studies on the mechanisms of sickness and clinical studies on the symptoms of sickness and depression that develop in patients treated with immunotherapy. Sickness behavior develops when the immune system is activated by pathogen- or damage-associated molecular patterns. It is a normal biological response to infection and cell injury. It helps the organism to mobilize its immune and metabolic defenses to fight the danger. Depression emerges on the background of sickness when the inflammatory response is too intense and long lasting or the resolution process is deficient. The transition from sickness to depression is mediated by activation of the kynurenine metabolism pathway that leads to the formation of neurotoxic kynurenine metabolites including quinolinic acid, an agonist of N-methyl-D-aspartate receptors. The neuroimmune processes and molecular factors that have been identified in the studies of inflammation-associated depression represent potential new targets for the development of innovative therapies for the treatment of major depressive disorders.

Indexed as

AnimalsDepressive DisorderHumansInflammationKynurenineMetabolic Networks and PathwaysNeuroimmunomodulationKynurenineBehaviorBrainCytokinesDepressionIndoleamine 2,3 dioxygenaseInflammationKynurenineMicrogliaNMDA receptorQuinolinic acidSickness

Identifiers

PMID27225497
PMCPMC6585430
OpenAlexW2396821322

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.