Uploaded July 2023 | Updated September 2026, 13 hours ago
Multiple sclerosis (MS) is a disease in which the immune system attacks a protective sheath, called myelin, which covers nerves in the central nervous system (CNS-brain and spinal cord). Myelin damage is referred 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 (called remyelination) after damage, but for unknown reasons, remyelination fails or is incomplete in MS. Efficient removal of myelin debris from the tissue after demyelination is a prerequisite to remyelination.
In the CNS, a specific cell type, microglia, can clear out myelin debris after damage. In MS lesions, microglial cells are activated and one of their functions is to pick up, digest and clear myelin debris (called phagocytosis). The mechanisms mediating microglia activation and phagocytosis are unknown.
Associate Professor Laura Piccio has been studying the role of TREM2, a protein located on the surface of microglia, in the phagocytosis of myelin debris and remyelination. The team’s preliminary results suggest that TREM2 plays a key function in these processes and that activation of TREM2 could enhance myelin debris clearance and remyelination.
The goal of this study is to investigate the molecular mechanisms supporting remyelination in the CNS with a specific focus on testing the effects of activating TREM2.
Multiple sclerosis (MS) is a disease in which the immune system attacks a protective sheath, called myelin, which covers nerves in the central nervous system (CNS-brain and spinal cord). Myelin damage is referred 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 (called remyelination) after damage, but for unknown reasons, remyelination fails or is incomplete in MS. Efficient removal of myelin debris from the tissue after demyelination is a prerequisite to remyelination.
In the CNS, a specific cell type, microglia, can clear out myelin debris after damage. In MS lesions, microglial cells are activated and one of their functions is to pick up, digest and clear myelin debris (called phagocytosis). The mechanisms mediating microglia activation and phagocytosis are unknown.
Associate Professor Laura Piccio has been studying the role of TREM2, a protein located on the surface of microglia, in the phagocytosis of myelin debris and remyelination. The team’s preliminary results suggest that TREM2 plays a key function in these processes and that activation of TREM2 could enhance myelin debris clearance and remyelination.
The goal of this study is to investigate the molecular mechanisms supporting remyelination in the CNS with a specific focus on testing the effects of activating TREM2.
