MS is a disease in which the immune system attacks the protective sheath that covers nerves in the central nervous system (CNS-brain and spinal cord), called myelin. Myelin damage is referred to as demyelination and the consequence is the disruption of communication between the brain and the rest of the body. The CNS has the potential to generate new myelin (remyelination) after damage, but for unknown reasons remyelination fails or is incomplete in MS. Efficient removal of the previously damaged myelin is a necessary prerequisite for repair to myelin to occur. In the CNS, a specific cell type called microglia, is capable of clearing out myelin debris after damage. In MS lesions, the site of damage in MS, microglial cells are activated and one of their functions is to pick up and digest damaged myelin. The mechanisms mediating microglia activation and digestion of myelin debris are not known.
Associate Professor Michael Buckland has been studying the role of TREM2, a protein made in microglia cells. In this project, he will study the possible role of TREM2 in regulating the functions of microglia cells and how it helps in clearing out damaged myelin.
Updated 22 January 2020
Updated: 21 January, 2020
Laboratory research that investigates scientific theories behind the possible causes, disease progression, ways to diagnose and better treat MS.
Research that builds on fundamental scientific research to develop new therapies, medical procedures or diagnostics and advances it closer to the clinic.
Clinical research is the culmination of fundamental and translational research turning those research discoveries into treatments and interventions for people with MS.