Abstract
Remyelination therapy for multiple sclerosis (MS) is a rapidly emerging research area despite the fact that only limited success has been achieved so far in clinical trials. The extracellular matrix (ECM) is significantly altered in chronic MS lesions, which is believed to be an important remyelination-inhibiting factor. However, the ECM components have not been specifically targeted in current MS remyelinating trials. Qin et al. (2017) described the role of a major ECM protein, fibronectin, in de/remyelination. Exogenous ganglioside GD1a was demonstrated to overcome the remyelination-inhibiting effects of aggregated fibronectin during later stages of oligodendrocyte maturation. Thus, GD1a could potentially be used as a novel remyelinating compound or as combination therapy in conjunction with other drugs to enhance different stages of remyelination in MS.
| Original language | English |
|---|---|
| Article number | e0435-17.2018 |
| Pages (from-to) | 1-4 |
| Number of pages | 4 |
| Journal | eNeuro |
| Volume | 5 |
| Issue number | 1 |
| DOIs |
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| Publication status | Published - 1 Jan 2018 |
Bibliographical note
Copyright the Author(s) 2018. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.Keywords
- Demyelination
- Extracellular matrix
- Multiple sclerosis
- Remyelination