Evidence map›Paper›PMID 21248132›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Genetically induced adult oligodendrocyte cell death is associated with poor myelin clearance, reduced remyelination, and axonal damage.

Hartmut B F Pohl, Cristina Porcheri, Thomas Mueggler, Lukas C Bachmann, Gianvito Martino, Dieter Riethmacher, Robin J M Franklin, Markus Rudin, Ueli Suter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 137 citations in OpenAlex.

  1. Article
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  8. Repeated ablations of mature Tmem10Cell death & disease · 2025
    Article
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  11. Review
  12. Article
  13. Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  14. Remyelination in the Central Nervous System.Cold Spring Harbor perspectives in biology · 2024
    Review
  15. Article
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  20. Review

19 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

9 authors at 7 institutions in 5 countries.

Hartmut B F PohlInstitute of Cell Biology, Department Biology, Eidgenössische Technische Hochschule (ETH) Zürich, CH-8093 Zürich, Switzerland.
Cristina Porcheri
Thomas Mueggler
Lukas C Bachmann
Gianvito Martino
Dieter Riethmacher
Robin J M Franklin
Markus Rudin
Ueli Suter
Vita-Salute San Raffaele University · ITBoard of the Swiss Federal Institutes of Technology · CHInstitute of Pharmacology · CZRichmont Graduate University · USUniversity of Cambridge · GBUniversity of Southampton · GBUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of oligodendrocytes is a feature of many demyelinating diseases including multiple sclerosis. Here, we have established and characterized a novel model of genetically induced adult oligodendrocyte death. Specific primary loss of adult oligodendrocytes leads to a well defined and highly reproducible course of disease development that can be followed longitudinally by magnetic resonance imaging. Histological and ultrastructural analyses revealed progressive myelin vacuolation, in parallel to disease development that includes motor deficits, tremor, and ataxia. Myelin damage and clearance were associated with induction of oligodendrocyte precursor cell proliferation, albeit with some regional differences. Remyelination was present in the mildly affected corpus callosum. Consequences of acutely induced cell death of adult oligodendrocytes included secondary axonal damage. Microglia were activated in affected areas but without significant influx of B-cells, T-helper cells, or T-cytotoxic cells. Analysis of the model on a RAG-1 (recombination activating gene-1)-deficient background, lacking functional lymphocytes, did not change the observed disease and pathology compared with immune-competent mice. We conclude that this model provides the opportunity to study the consequences of adult oligodendrocyte death in the absence of primary axonal injury and reactive cells of the adaptive immune system. Our results indicate that if the blood-brain barrier is not disrupted, myelin debris is not removed efficiently, remyelination is impaired, and axonal integrity is compromised, likely as the result of myelin detachment. This model will allow the evaluation of strategies aimed at improving remyelination to foster axon protection.

Indexed as

AnimalsAxonsCell CountCell DeathCorpus CallosumDisease ProgressionFluorescent Antibody TechniqueMagnetic Resonance ImagingMiceMice, TransgenicMicrogliaMicroscopy, ElectronMyelin SheathOligodendrogliaRotarod Performance Test

Identifiers

PMID21248132
PMCPMC6632929
OpenAlexW2117823483

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.