Journal
NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms13275
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Funding
- German Federal Ministry of Research and Education (BMBF
- Competence Network Multiple Sclerosis)
- European Research Council under the European Union's Seventh Framework Program (FP
- ERC) [310932, 616791]
- Verein Therapieforschung fur MS-Kranke e.V.
- Center for Integrated Protein Science Munich (CIPSM) [EXC 114]
- German-Israeli Foundation
- Munich Center for Systems Neurology (SyNergy) [EXC 1010]
- DFG Priority Program 1710
- DFG Collaborative Research Centre [Transregio 128]
- Hertie-Foundation (Myelin Repair Foundation)
- DFG (Collaborative Research Center 870)
- Swiss National Science Foundation [PP00P3_152928]
- Klaus-Tschira Foundation
- Gebert-Ruf Foundation
- Swiss MS Society
- Swiss National Science Foundation (SNF) [PP00P3_152928] Funding Source: Swiss National Science Foundation (SNF)
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Oligodendrocyte damage is a central event in the pathogenesis of the common neuro-inflammatory 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.
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