Understanding the molecular basis of myelin repair
In Multiple Sclerosis (MS), oligodendrocytes are often found within demyelinated lesions, but these fail to remyelinate the demyelinated axons. Indeed, one of the major factors contributing to disease progression is this ‘remyelination block’, where the process of oligodendrocyte differentiation and myelination is inhibited in demyelinating lesions.
Our research has begun to directly investigate the molecular basis of this inhibition of myelin repair. Wnts are secreted proteins that control many different aspects of cell development and behaviour. Key components of the Wnt signalling pathway are upregulated in MS lesions, strongly suggesting that this pathway could be one of the factors that limits oligodendrocyte differentiation and remyelination in the context of MS. This project involves the analysis of transgenic mice that have the Wnt signalling pathway specifically perturbed in oligodendrocytes. We are interested in identifying the precise influence that Wnt signalling exerts upon normal myelination during development. In addition, adopting animal models of demyelinating disease, we are also interested in identifying the precise influence that Wnt signalling exerts upon remyelination following a demyelinating insult in vivo, and whether blocking Wnt signalling can enhance myelin repair.
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