Evidence map›Paper›PMID 26067430›Full record

ArticleJournal of molecular neuroscience : MN2015

Anatomical Distribution of Cuprizone-Induced Lesions in C57BL6 Mice.

Johannes Goldberg, Tim Clarner, Cordian Beyer, Markus Kipp

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. Fisetin Mitigates Ferroptosis and Promotes Remyelination in a Cuprizone Model of Multiple Sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  4. Article
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  6. Article
  7. Article
  8. Article
  9. How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Johannes GoldbergInstitute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany.
Tim ClarnerInstitute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany.
Cordian BeyerInstitute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany.
Markus KippDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany. mkipp@ukaachen.de.
RWTH Aachen University · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although multiple sclerosis (MS) has been considered a white matter disease, MS lesions occur frequently in the gray matter parts of the brain. Gray matter demyelination and atrophy are found during earliest disease stages, and a growing body of evidence demonstrates a positive correlation between gray matter pathology and various measures of motor disability and cognitive impairment. The cuprizone model is classically regarded as white matter demyelination model. However, recent evidence suggests that different gray matter areas are also affected. In this study, we address the vulnerability of white and gray matter forebrain regions in the cuprizone model. While the corpus callosum as interhemispheric white matter tract is affected in this model, other white matter tracts such as the mammillo-thalamic tract, the columns of the fornix, the stria terminalis, the optic tract, or hippocampal fimbria do not present overt demyelination after 5-week cuprizone intoxication. In contrast, gray matter demyelination is widespread in this model. Furthermore, vulnerable white matter tracts display extensive acute axonal damage. These results highlight the relevance of the cuprizone model to study MS-related gray matter pathology and neurodegeneration.

Indexed as

AnimalsAxonsCorpus CallosumCuprizoneDemyelinating DiseasesGray MatterMiceMice, Inbred C57BLMonoamine Oxidase InhibitorsMyelin SheathWhite MatterCuprizoneMonoamine Oxidase InhibitorsAxonal damageCuprizoneDemyelinationGray matterMicrogliaNeurodegenerationWhite matter

Identifiers

PMID26067430
OpenAlexW1905230752

What OpenQuestion holds

Textmetadata
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.