Evidence map›Paper›PMID 29873041›Full record

ArticleMolecular neurobiology2019

G-Protein-Coupled Receptor Gpr17 Expression in Two Multiple Sclerosis Remyelination Models.

Stella Nyamoya, Patrizia Leopold, Birte Becker, Cordian Beyer, Fabian Hustadt, Christoph Schmitz, Anne Michel, Markus Kipp

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Advances in Therapeutics Research for Demyelinating Diseases.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  5. Review
  6. Review
  7. GPR17 modulates anxiety-like behaviorsActa pharmaceutica Sinica. B · 2024
    Article
  8. Article
  9. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Myelin Repair: From Animal Models to Humans.Frontiers in cellular neuroscience · 2021
    Review
  14. Macroglial diversity: white and grey areas and relevance to remyelination.Cellular and molecular life sciences : CMLS · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 2 countries.

Stella NyamoyaInstitute of Neuroanatomy and JARA-BRAIN, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany.
Patrizia LeopoldDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany.
Birte BeckerInstitute of Neuroanatomy and JARA-BRAIN, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany.
Cordian BeyerInstitute of Neuroanatomy and JARA-BRAIN, Faculty of Medicine, RWTH Aachen University, 52074, Aachen, Germany.
Fabian HustadtNeurosciences TA Biology, UCB BioPharma, Braine L'Alleud, Brussels, Belgium.
Christoph SchmitzDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany.
Anne MichelNeurosciences TA Biology, UCB BioPharma, Braine L'Alleud, Brussels, Belgium.
Markus KippDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany. markus.kipp@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DERWTH Aachen University · DEUCB Pharma (Belgium) · BE

Funding

Deutsche Forschungsgemeinschaft KI 1469/8-1
6 · The paper itself

Abstract

In multiple sclerosis patients, demyelination is prominent in both the white and gray matter. Chronic clinical deficits are known to result from acute or chronic injury to the myelin sheath and inadequate remyelination. The underlying molecular mechanisms of remyelination and its failure remain currently unclear. Recent studies have recognized G protein-coupled receptor 17 (GPR17) as an important regulator of oligodendrocyte development and remyelination. So far, the relevance of GPR17 for myelin repair was mainly tested in remyelinating white matter lesions. The relevance of GPR17 for gray matter remyelination as well as remyelination of chronic white matter lesions was not addressed so far. Here, we provide a detailed characterization of GPR17 expression during experimental de- and remyelination. Experimental lesions with robust and limited endogenous remyelination capacity were established by either acute or chronic cuprizone-induced demyelination. Furthermore, remyelinating lesions were induced by the focal injection of lysophosphatidylcholine (LPC) into the corpus callosum. GPR17 expression was analyzed by complementary techniques including immunohistochemistry, in situ hybridization, and real-time PCR. In control animals, GPR17

Indexed as

AnimalsCerebral CortexCorpus CallosumCuprizoneDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGray MatterMaleMiceMultiple SclerosisMyelin SheathNerve Tissue ProteinsReceptors, G-Protein-CoupledRemyelinationCuprizoneGPR17 protein, mouseNerve Tissue ProteinsReceptors, G-Protein-CoupledCNSCuprizoneGpr17LPCMultiple sclerosisRemyelination

Identifiers

PMID29873041
OpenAlexW2806410655

What OpenQuestion holds

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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.