Evidence map›Paper›PMID 19349355›Full record

ArticleThe American journal of pathology2009

Statin therapy inhibits remyelination in the central nervous system.

Veronique E Miron, Simone P Zehntner, Tanja Kuhlmann, Samuel K Ludwin, Trevor Owens, Timothy E Kennedy, Barry J Bedell, Jack P Antel

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

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  15. Delayed atorvastatin delivery promotes recovery after experimental spinal cord injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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10 more citing papers are in PubMed but not listed here.

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 4 institutions in 5 countries.

Veronique E MironNeuroimmunology Unit, the Centre for Neuronal Survival, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
Simone P Zehntner
Tanja Kuhlmann
Samuel K Ludwin
Trevor Owens
Timothy E Kennedy
Barry J Bedell
Jack P Antel
Montreal Neurological Institute and Hospital · CAMcGill University · CAQueen's University · CAUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Remyelination of lesions in the central nervous system contributes to neural repair following clinical relapses in multiple sclerosis. Remyelination is initiated by recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating oligodendrocytes. Simvastatin, a blood-brain barrier-permeable statin in multiple sclerosis clinical trials, has been shown to impact the in vitro processes that have been implicated in remyelination. Animals were fed a cuprizone-supplemented diet for 6 weeks to induce localized demyelination in the corpus callosum; subsequent return to normal diet for 3 weeks stimulated remyelination. Simvastatin was injected intraperitoneally during the period of coincident demyelination and OPC maturation (weeks 4 to 6), throughout the entire period of OPC responses (weeks 4 to 9), or during the remyelination-only phase (weeks 7 to 9). Simvastatin treatment (weeks 4 to 6) caused a decrease in myelin load and both Olig2(strong) and Nkx2.2(strong) OPC numbers. Simvastatin treatment (weeks 4 to 9 and 7 to 9) caused a decrease in myelin load, which was correlated with a reduction in Nkx2.2(strong) OPCs and an increase in Olig2(strong) cells, suggesting that OPCs were maintained in an immature state (Olig2(strong)/Nkx2.2(weak)). NogoA+ oligodendrocyte numbers were decreased during all simvastatin treatment regimens. Our findings suggest that simvastatin inhibits central nervous system remyelination by blocking progenitor differentiation, indicating the need to monitor effects of systemic immunotherapies that can access the central nervous system on brain tissue-repair processes.

Indexed as

AnimalsAnticholesteremic AgentsBasic Helix-Loop-Helix ProteinsBlotting, WesternCell DifferentiationCell ProliferationChelating AgentsCuprizoneDemyelinating DiseasesFlow CytometryFluorescent Antibody TechniqueHomeobox Protein Nkx-2.2Homeodomain ProteinsImmunoenzyme TechniquesMaleMiceAnticholesteremic AgentsBasic Helix-Loop-Helix ProteinsChelating AgentsCuprizoneHomeobox Protein Nkx-2.2Homeodomain ProteinsNerve Tissue Proteinsnkx2.2b protein, zebrafishNkx2-2 protein, mouseOlig2 protein, mouseOligodendrocyte Transcription Factor 2RNA, MessengerSimvastatinTranscription FactorsZebrafish Proteins

Identifiers

PMID19349355
PMCPMC2671276
OpenAlexW2098613224

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.