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, Alexander Ghanem, Karl-Klaus Conzelmann, Imke Metz, Wolfgang Brück, Matthew Routh, Mikael Simons, Derron Bishop, Thomas Misgeld () and Martin Kerschensteiner ()
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Elisa Romanelli: Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich
Doron Merkler: University of Geneva
Aleksandra Mezydlo: Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich
Marie-Theres Weil: Max-Planck Institute of Experimental Medicine
Martin S. Weber: Georg-August University Göttingen
Ivana Nikić: Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich
Stephanie Potz: Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich
Edgar Meinl: Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich
Florian E. H. Matznick: Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich
Mario Kreutzfeldt: University of Geneva
Alexander Ghanem: Max von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians University Munich
Karl-Klaus Conzelmann: Max von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians University Munich
Imke Metz: Institute of Neuropathology, Georg-August University Göttingen
Wolfgang Brück: Institute of Neuropathology, Georg-August University Göttingen
Matthew Routh: Ball State University
Mikael Simons: Max-Planck Institute of Experimental Medicine
Derron Bishop: Indiana University School of Medicine
Thomas Misgeld: German Center for Neurodegenerative Diseases (DZNE)
Martin Kerschensteiner: Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms13275

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