Myelin regeneration in demyelinating disorders: new developments in biology and clinical pathology

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Purpose of review

The following article reviews recent advances in remyelination biology and its presentation in demyelinating diseases such as multiple sclerosis. It is based primarily on articles published during 2006.

Recent findings

The principal themes are the identity and properties of remyelinating cells; the role of inflammation in remyelination; and the complexity of and redundancy within the signalling environment regulating remyelination.


Central nervous system remyelination is mainly mediated by oligodendrocyte precursor cells, although subventricular zone-derived cells contribute to the repair of periventricular lesions. Oligodendrocyte precursor cells may differentiate into astrocytes and Schwann cells following injury and exhibit more stem cell-like features than previously recognized. A complex matrix of environmental factors, including cytokines, chemokines and growth factors, act upon oligodendrocyte precursor cells, causing their activation and eventual differentiation into remyelinating oligodendrocytes. Inflammatory cells contribute by providing components of the signalling matrix and by the phagocytic removal of myelin debris. Many factors within the signalling environment have redundant functions – a feature of regeneration with implications for developing remyelination therapies. Advances in remyelination biology have been accompanied by more detailed analyses of remyelination in multiple sclerosis and important translational developments, including the ability to identify myelin by positron emission tomography.

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