Why is your research important and how will it influence the understanding and treatment of MS?
We pioneered work that identified that the neurotrophin brain-derived neurotrophic factor (BDNF) promotes myelination during development, acting directly on the myelin producing cells called oligodendrocytes. This led us to the view that BDNF might also promote myelin repair after injury, such as occurs in MS. In collaboration with others, we developed a drug-like mimetic of BDNF and identified that it indeed could promote myelin repair in a mouse model of central demyelination. However, these studies were executed in a permissive environment, where spontaneous remyelination occurs - in relatively young animals after a single bout of demyelination. This is not the environment in which myelin repair must occur in multiple sclerosis - in a more mature nervous system that has a less permissive environment. The innovative aspect of this study is that we have manipulated the experimental model to include repeated bouts of demyelination in older mice to develop a demyelinated environment that does not spontaneously remyelinate. This adaptation more closely approximates the environment in which remyelination must occur in multiple sclerosis. Examining the efficacy of our BDNF mimetic in this environment is a small but significant step towards identifying whether this is a rational approach to cure MS.