Remyelination in the CNS: from biology to therapy

@article{Franklin2008RemyelinationIT,
  title={Remyelination in the CNS: from biology to therapy},
  author={Robin J. M. Franklin and Charles ffrench‐Constant},
  journal={Nature Reviews Neuroscience},
  year={2008},
  volume={9},
  pages={839-855}
}
Remyelination involves reinvesting demyelinated axons with new myelin sheaths. In stark contrast to the situation that follows loss of neurons or axonal damage, remyelination in the CNS can be a highly effective regenerative process. It is mediated by a population of precursor cells called oligodendrocyte precursor cells (OPCs), which are widely distributed throughout the adult CNS. However, despite its efficiency in experimental models and in some clinical diseases, remyelination is often… 
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TLDR
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TLDR
The pathophysiological nature of remyelination failure in chronic MS is examined and the role of TIP30 as a novel therapeutic target is discussed, which inhibits proper nucleocytoplasmic transport and thus disables nuclear import of transcription factors that are required for differentiation.
The Molecular Basis for Remyelination Failure in Multiple Sclerosis
TLDR
The molecular factors contributing to remyelination failure in MS are reviewed by inhibiting OPC and NSC differentiation or modulating microglial behavior.
Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination
TLDR
Remyelination strategies should, therefore, focus on stimulation of differentiation or prevention of apoptosis, as well as establishment of a supportive environment for OPC-mediated remyelination, which may be especially important in chronically demyelinated lesions.
Enhancing remyelination in disease--can we wrap it up?
TLDR
A model is proposed that may help to provide cues for how remyelination can be therapeutically enhanced in clinical disease and is critically evaluates recent advances in understanding of the biology of oligodendrocyte precursor cells and of the stage-dependent molecular pathology of multiple sclerosis lesions relevant to the regeneration of myelin sheaths.
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TLDR
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