Journal
JOURNAL OF CELL BIOLOGY
Volume 206, Issue 3, Pages 335-345Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201404154
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Funding
- German Research Foundation [SI 746/9-1, 10-1, TRR43]
- Tschira-Stiftung
- E-Rare program (German Federal Ministry of Research and Education)
- Center for Integrated Protein Science (Munich) [EXC 114]
- Deutsche Forschungsgemeinschaft (DFG) [SFB 870]
- European Research Council (ERC) under the European Union's [6167911]
- German Center for Neurodegenerative Disease (Munich)
- DFG [Transregio 128]
- ERC under the European Union's [3109321]
- Hertie Foundation
- Verein Therapieforschung far MS-Kranke e.V.
- Munich Center for Systems Neurology (SyNergy) [EXC 1010]
- DFG Priority Program [1710]
- German Federal Ministry of Research and Education (Competence Network on Multiple Sclerosis)
Ask authors/readers for more resources
Demyelination and axon loss are pathological hall-marks of the neuroinflammatory disorder multiple sclerosis (MS). Although we have an increasingly detailed understanding of how immune cells can damage axons and myelin individually, we lack a unified view of how the axon-myelin unit as a whole is affected by immunemediated attack. In this review, we propose that as a result of the tight cell biological interconnection of axons and myelin, damage to either can spread, which might convert a local inflammatory disease process early in MS into the global progressive disorder seen during later stages. This mode of spreading could also apply to other neurological disorders.
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