Evidence map›Paper›PMID 27848954›Full record

ArticleNature communications2016

Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model.

Elisa Romanelli, Doron Merkler, Aleksandra Mezydlo, Marie-Theres Weil, Martin S Weber, Ivana Nikić, Stephanie Potz, Edgar Meinl, Florian E H Matznick, Mario Kreutzfeldt and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
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  3. Disruption to TFEB signaling and autophagy in newly formed oligodendrocytes leads to aberrant generation of CNS myelin.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

19 authors at 7 institutions in 3 countries.

Elisa RomanelliInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Doron MerklerDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva, Switzerland.
Aleksandra MezydloInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Marie-Theres WeilMax-Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Martin S WeberDepartment of Neurology, Georg-August University Göttingen, 37075 Göttingen, Germany.
Ivana NikićInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Stephanie PotzInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Edgar MeinlInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Florian E H MatznickInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Mario KreutzfeldtDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva, Switzerland.
Alexander GhanemMax von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Karl-Klaus ConzelmannMax von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Imke MetzInstitute of Neuropathology, Georg-August University Göttingen, 37075 Göttingen, Germany.
Wolfgang BrückInstitute of Neuropathology, Georg-August University Göttingen, 37075 Göttingen, Germany.
Matthew RouthDepartment of Physiology and Health Science, Ball State University, Muncie, Indiana 47306, USA.
Mikael SimonsMax-Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.
Derron BishopDepartment of Cellular and Integrative Physiology and Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Thomas MisgeldGerman Center for Neurodegenerative Diseases (DZNE), 81377 Munich, Germany.
Martin KerschensteinerInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Ludwig-Maximilians-Universität München · DEUniversity of Göttingen · DEUniversity of Geneva · CHBall State University · USGerman Center for Neurodegenerative Diseases · DEIndiana University – Purdue University Indianapolis · USMax Planck Institute of Experimental Medicine · DE

Funding

European Research Council
6 · The paper itself

Abstract

Oligodendrocyte damage is a central event in the pathogenesis of the common neuroinflammatory condition, multiple sclerosis (MS). Where and how oligodendrocyte damage is initiated in MS is not completely understood. Here, we use a combination of light and electron microscopy techniques to provide a dynamic and highly resolved view of oligodendrocyte damage in neuroinflammatory lesions. We show that both in MS and in its animal model structural damage is initiated at the myelin sheaths and only later spreads to the oligodendrocyte cell body. Early myelin damage itself is characterized by the formation of local myelin out-foldings-'myelinosomes'-, which are surrounded by phagocyte processes and promoted in their formation by anti-myelin antibodies and complement. The presence of myelinosomes in actively demyelinating MS lesions suggests that oligodendrocyte damage follows a similar pattern in the human disease, where targeting demyelination by therapeutic interventions remains a major open challenge.

Indexed as

AnimalsAntibodiesComplement System ProteinsDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansImaging, Three-DimensionalMacrophagesMice, Inbred C57BLMultiple SclerosisMyelin SheathOligodendrogliaOpsonin ProteinsOrganellesAntibodiesComplement System ProteinsOpsonin Proteins

Identifiers

PMID27848954
PMCPMC5116090
OpenAlexW2554354789

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.