The idea that there was a real possibility of making a meaningful contribution to the lives of people with multiple sclerosis (MS) during my scientific career. In other words: to be involved in solving a challenging but solvable problem that, if cracked, would unequivocally be of benefit to a significant number of people.

Undoubtedly, the advent of immunomodulatory therapies that unequivocally benefit people with relapsing remitting disease. We now need to extend those advances to make sure that people with progressive MS also benefit.

This project aims to improve treatments for MS. Our research focuses on a protein called Mertk, which helps control the immune system's actions in the brain. We want to understand how Mertk affects MS and identify which patients might see the most benefit from treatments that target this protein. We will carry out studies involving both people and mice. By looking at blood samples from patients with MS, we will explore how changes in the levels of Mertk are linked with the activity of the disease.

We will also use mice to see how changes in Mertk might influence symptoms of MS, such as weakness and loss of coordination. The information we gather will help us determine which patients have certain versions of the Mertk protein. This could allow doctors to choose treatments more likely to help those patients, making the treatments more effective and possibly reducing side effects.

Current therapies for MS generally target lymphocytes non-specifically, without preventing progressive disability. More personalised, precision-based therapies are needed. With this in mind, we have identified genetic and molecular markers for personal risk stratification in MS. Notably, the influence of the protein, Mertk, differs according to minor variations in the gene that encodes it. Within the central nervous system (CNS), Mertk assists innate immune cells to clear myelin debris, which is necessary for repair. However, in some patients with particular variations in the Mertk gene, Mertk might also increase blood-borne T lymphocyte activation, to promote disease activity. We believe that inhibiting Mertk in the blood could benefit those patients predisposed to high levels of Mertk expression on disease promoting T lymphocytes. We aim to prove that targeted Mertk inhibition can precisely and effectively reduce MS activity and progression with fewer side effects, and thereby advance the important concept of personalised therapy for MS.

The most enjoyable feature is the thrill of discovery and developing the vision of how that discovery might be translated into something of meaningful benefit. The biggest challenge remains the battle to acquire the funding to maintain that pipeline of discovery and to be able to continue to support the career development of the next generation of scientists. That is why the continuing support of MS Australia is so important, not only to my laboratory but to the field in general.