Evidence map›Paper›PMID 23916895›Full record

ArticleBrain, behavior, and immunity2014

Dysregulation in myelination mediated by persistent neuroinflammation: possible mechanisms in chemotherapy-related cognitive impairment.

Teresita L Briones, Julie Woods

Open access · hybridAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
4.3field-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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
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  8. Transcranial photobiomodulation for the treatment of chemobrain: new perspectives from a pilot study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
    Article
  9. Article
  10. Review
  11. Cognitive dysfunction in chemobrain: Molecular mechanisms and therapeutic implications.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Review
  12. Article
  13. Article
  14. Review
  15. Perturbations in the neuroactive ligand-receptor interaction and renin angiotensin system pathways are associated with cancer-related cognitive impairment.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025
    Article
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  17. Article
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6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Teresita L BrionesDepartment of Adult Health, Wayne State University, Detroit, MI 48202, USA. Electronic address: tbriones@wayne.edu.
Julie Woods
University of Illinois Chicago · USWayne State University · US

Funding

GENE EXPRESSION-ENVIRONMENT LINK IN CEREBRAL ISCHEMIAR01NR007666 · NINR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BRIONES, TERESITA L · 2002 to 2006
$1.4M
NINR NIH HHS R01 NR007666
6 · The paper itself

Abstract

Cognitive impairment is commonly reported as a consequence of chemotherapy and can have considerable impact on everyday life on cancer patients. Thus, it is imperative to have a clear understanding of this phenomenon and the underlying mechanism involved. In the present study we examined the role of neuroinflammation and myelination in chemotherapy-related cognitive impairment. Female Sprague-Dawley rats (12-months old) were used in the study (total n=52, 13rats/group). Rats were randomly assigned to either the chemotherapy or saline control group. The drug combination of cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) was given i.p. once a week for 4weeks. Rats in the control group received normal saline of equal volume. Animals from each group were further randomized to receive either: cyclooxygenase (COX-2) inhibitor, NS-393, to block the inflammatory response or vehicle. NS-398 was given at 10mg/kg i.p. and equal volume of saline (vehicle) was injected i.p. as vehicle. Both NS-398 and vehicle were injected 1h after the first CMF dose and then given daily for 28days then rats were tested in the Y maze. Our data showed that: (1) CMF led to the increase in the levels of inflammatory mediators IL-1β, TNF-α, and COX-2 while levels of the anti-inflammatory cytokine IL-10 decreased; (2) cognitive impairment and neuroinflammation resulting from CMF persisted 4weeks after the treatment ended; and (3) administration of NS-398 attenuated CMF-induced neuroinflammation and effects on myelin and cognitive impairment. These findings suggest the involvement of neuroinflammation in CMF-induced changes in myelin and myelination, and cognitive impairment.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsCognition DisordersCorpus CallosumCyclophosphamideCytokinesFemaleFluorouracilInflammationMethotrexateNerve Fibers, MyelinatedRandom AllocationRatsRats, Sprague-DawleyRecognition, PsychologyCyclophosphamideCytokinesFluorouracilMethotrexateCorpus callosumCOX-2IL-10IL-1betaTNF-alpha

Identifiers

PMID23916895
PMCPMC3858476
OpenAlexW2025046102

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.