Evidence map›Paper›PMID 30607821›Full record

ArticleMetabolic brain disease2019

Evaluation strategy to determine reliable demyelination in the cuprizone model.

Uta Chrzanowski, Christoph Schmitz, Anja Horn-Bochtler, Anne Nack, Markus Kipp

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Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Science (New York, N.Y.) · 2024
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. 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

5 authors.

Uta ChrzanowskiDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany.
Christoph SchmitzDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany.
Anja Horn-BochtlerDepartment of Anatomy I, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany.
Anne NackDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany.
Markus KippDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany. markus.kipp@med.uni-rostock.de.ORCID http://orcid.org/0000-0001-5043-9052

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In multiple sclerosis patients, chronic clinical deficits are known to result from axonal degeneration which is triggered by inadequate remyelination. The underlying molecular mechanisms of remyelination and its failure remain currently unclear. In vivo models, among the cuprizone model, are valuable tools to study underlying mechanisms of remyelination and its failure. Since complete and reproducible demyelination of the analyzed brain region is an indispensable prerequisite for efficient remyelination experiments, in this study we systematically addressed which part of the corpus callosum is reliably and consistently demyelinated after acute cuprizone-induced demyelination. Following a novel evaluation strategy, we can show that at the level of the rostral hippocampus, the most medial sectors of the corpus callosum (spanning 500 μm in the horizontal plane) are consistently demyelinated, whereas more lateral sectors show inconsistent and incomplete demyelination. These results precisely define a part of the corpus callosum which should be used as a region of interest during remyelination experiments.

Indexed as

AnimalsBrainCuprizoneDemyelinating DiseasesDisease Models, AnimalMaleMice, Inbred C57BLMyelin Basic ProteinMyelin SheathOligodendrogliaCuprizoneMyelin Basic ProteinCuprizoneDemyelinationOptical densityRegenerationRemyelination

Identifiers

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Registered trials

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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.