The aim of this project is to promote functional recovery of CNS neurons following acute traumatic and/or chronic inflammatory injury. Our goal is to identify new molecular targets and develop novel therapeutics that promote:
- neuroprotection,
- neuroregeneration and
- remyelination of damaged CNS tissue
The primary focus of this project is to discover new regenerative treatments for neuroinflammatory disorders of the brain and spinal cord, such as Multiple Sclerosis (MS). Myelin-forming glial cells that wrap and insulate neurons become damaged in MS and this renders axons exposed and vulnerable to degeneration. This demyelination and eventual loss of axons is what leads to the debilitating symptoms of MS, including blurred vision, fatigue, limb weakness and problems with balance.
Neurons of the adult CNS generally display very limited regeneration after injury. In contrast, glial cells such as myelinating oligodendrocytes are replenished from a pool of adult neural stem cells, termed oligodendrocyte precursor cells (OPCs). Therefore, our CNS has the ability to repair itself and remyelinate damaged axons.
Our researchers study the intrinsic mechanisms underlying this CNS regeneration. By understanding how remyelination occurs naturally in the brain and spinal cord, we aim to develop methods to enhance the efficiency of endogenous adult stem/precursor cell types to repair lesioned tissue.
Like all regenerative processes, however, remyelination progressively declines as we age. The mechanisms underlying this deterioration in myelin repair capacity are not fully understood. Therefore, a goal of this project is to understand this natural age-related decline in remyelination in order to find ways to promote the regenerative capacity of adult stem/precursor cells in the CNS.