Evidence map›Paper›PMID 28381594›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis.

Andrea Schampel, Oleg Volovitch, Tobias Koeniger, Claus-Jürgen Scholz, Stefanie Jörg, Ralf A Linker, Erhard Wischmeyer, Marie Wunsch, Johannes W Hell, Süleyman Ergün and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Cell death in multiple sclerosis.Cell death and differentiation · 2026
    Review
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  18. Disturbed Presynaptic CaiScience · 2020
    Article
  19. Article
  20. Modulating microglia activation prevents maternal immune activation induced schizophrenia-relevant behavior phenotypes via arginase 1 in the dentate gyrus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    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

11 authors at 5 institutions in 2 countries.

Andrea SchampelDepartment of Anatomy and Cell Biology, University of Würzburg, 97070 Wuerzburg, Germany.
Oleg VolovitchDepartment of Anatomy and Cell Biology, University of Cologne, 50931 Cologne, Germany.
Tobias KoenigerDepartment of Anatomy and Cell Biology, University of Würzburg, 97070 Wuerzburg, Germany.
Claus-Jürgen ScholzCore Unit Systems Medicine, University Hospital of Würzburg, 97080 Wuerzburg, Germany.
Stefanie JörgDepartment of Neurology, Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany.
Ralf A LinkerDepartment of Neurology, Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany.
Erhard WischmeyerInstitute of Physiology, Molecular Electrophysiology, University of Würzburg, 97070 Wuerzburg, Germany.
Marie WunschDepartment of Anatomy and Cell Biology, University of Würzburg, 97070 Wuerzburg, Germany.
Johannes W HellDepartment of Pharmacology, University of California, Davis, CA 95616.
Süleyman ErgünDepartment of Anatomy and Cell Biology, University of Würzburg, 97070 Wuerzburg, Germany.
Stefanie KuertenDepartment of Anatomy and Cell Biology, University of Würzburg, 97070 Wuerzburg, Germany; stefanie.kuerten@fau.de.ORCID 0000-0001-6119-605X
University of Würzburg · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of Bonn · DEUniversity of California, Davis · USUniversity of Cologne · DE

Funding

Role of a-actinin in Cav1.2 FunctionR01AG055357 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI JOHANNES W HELL · 2016 to 2026
$4.0M
NIA NIH HHS R01 AG055357
6 · The paper itself

Abstract

Despite continuous interest in multiple sclerosis (MS) research, there is still a lack of neuroprotective strategies, because the main focus has remained on modulating the immune response. Here we performed in-depth analysis of neurodegeneration in experimental autoimmune encephalomyelitis (EAE) and in in vitro studies regarding the effect of the well-established L-type calcium channel antagonist nimodipine. Nimodipine treatment attenuated clinical EAE and spinal cord degeneration and promoted remyelination. Surprisingly, we observed calcium channel-independent effects on microglia, resulting in apoptosis. These effects were cell-type specific and irrespective of microglia polarization. Apoptosis was accompanied by decreased levels of nitric oxide (NO) and inducible NO synthase (iNOS) in cell culture as well as decreased iNOS and reactive oxygen species levels in EAE. In addition, increased numbers of Olig2

Indexed as

Disease Models, AnimalAnimalsApoptosisCalcium Channels, L-TypeCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalMiceMicrogliaMultiple SclerosisNimodipineNitric Oxide Synthase Type IIOligodendrogliaReactive Oxygen SpeciesRemyelinationSpinal CordCalcium Channels, L-TypeNimodipineNitric Oxide Synthase Type IIReactive Oxygen SpeciesEAEmicrogliaMSneuroprotectionnimodipine

Identifiers

PMID28381594
PMCPMC5402421
OpenAlexW2604716987

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.