Targeting the molecular mechanisms of axonal degeneration, demyelination and remyelination in multiple sclerosis

Multiple sclerosis (MS) is a neurodegenerative condition that can lead to life-long disability in the predominantly female population of less than 40 years of age. In contrast to the original focus of research on the autoimmune mechanisms that are operative in MS, there is now clear evidence that axonal damage/loss is the major arbiter of profound neurological deficit in MS sufferers. This thesis aimed to investigate the neuroprotective mechanism in MS by (i)identifying the potential molecular targets that govern axonal damage, (ii) devising experimental methods to directly protect axons during neuroinflammation and (iii) investigating therapeutic strategies for the re-formation of the myelin sheath (remyelination) to protect axons from secondary damage upon demyelination.