Myelin plays a vital role in neurologic function and its loss in multiple sclerosis (MS) often results in severe clinical disability; remyelination is a critical repair mechanism in many neurologic disorders including MS, hence a complete understanding of this process and how it can be promoted are vital to devising urgently needed therapeutic strategies. There is also a critical need for noninvasive testing to follow these changes in life and help the development of novel therapeutics that promote myelin repair and neuroprotection. In this project we are investigating a highly novel animal model of CNS demyelination and remyelination which is promoted by treatment with vitamin B12. We are investigating the basic features of this model, including the origin(s) of the cellular response that results in remyelination, the differential gene expression associated with all stages of the disease process, whether remyelination protects axons from later degeneration, whether remyelination can be identified by novel, quantitative MRI methods as well as evoked potentials, and whether failure of remyelination in chronic disease leads to axon loss detected by these modalities. The project will lead to a greater understanding of how quantitative MRI methods, such as magnetization transfer imaging, reflect the cellular and molecular changes taking place during demyelination and remyelination.
April 2016 to March 2019
This project led by: Ian Duncan, PhD