4.7 Review

A unified cell biological perspective on axon-myelin injury

Journal

JOURNAL OF CELL BIOLOGY
Volume 206, Issue 3, Pages 335-345

Publisher

ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201404154

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Funding

  1. German Research Foundation [SI 746/9-1, 10-1, TRR43]
  2. Tschira-Stiftung
  3. E-Rare program (German Federal Ministry of Research and Education)
  4. Center for Integrated Protein Science (Munich) [EXC 114]
  5. Deutsche Forschungsgemeinschaft (DFG) [SFB 870]
  6. European Research Council (ERC) under the European Union's [6167911]
  7. German Center for Neurodegenerative Disease (Munich)
  8. DFG [Transregio 128]
  9. ERC under the European Union's [3109321]
  10. Hertie Foundation
  11. Verein Therapieforschung far MS-Kranke e.V.
  12. Munich Center for Systems Neurology (SyNergy) [EXC 1010]
  13. DFG Priority Program [1710]
  14. German Federal Ministry of Research and Education (Competence Network on Multiple Sclerosis)

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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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