Multiple sclerosis (MS) is one of the most common causes of disability in young adults. In MS, the immune system mistakenly attacks myelin—the protective coating around nerve fibres—disrupting nerve signals and leading to disability as nerves degenerate. While the body can repair myelin through a process called remyelination, this ability declines with age. My project focuses on understanding why remyelination becomes less effective and exploring strategies to promote myelin repair in people with MS.

One of the key elements of the project focuses on a completed clinical trial testing whether a combination of two existing drugs—metformin and clemastine—can help repair myelin. Using MRI scans and visual system tests, I will assess whether specific brain regions respond more effectively to treatment and refine how remyelination is measured in clinical studies.

Another important aspect of my research is understanding why some people with MS repair myelin better than others. I am studying a large group of individuals, including children and adults, to see how age and other factors influence this ability. I will also explore whether better myelin repair helps protect nerve cells from long-term damage. By tracking myelin repair and neuroprotection over time, we can identify who might benefit most from remyelinating treatments.

Finally, I am investigating new ways to measure remyelination using eye-tracking technology. This method could provide a faster, more sensitive way to assess myelin repair compared to traditional techniques. If successful, this could help speed up the development of new therapies.

The primary objective of the research is to identify the best ways to promote and measure remyelination in people with MS. This is a leading strategy to protect nerves from ongoing damage and prevent progression of disability.