Multiple sclerosis (MS) is a debilitating neurodegenerative autoimmune disease, affecting more than 350,000 people in the US and millions worldwide. Multiple sclerosis (MS) is a disease of the central nervous system (CNS) in which the neuron encapsulating myelin sheath is destroyed. Myelin has the dual role of insulating axons in order to permit rapid transmission of nerve impulses and shield axons from harm. Although the etiology of MS is poorly understood, it is now clear that both genetic and environmental factors are involved. The main destructive force in MS is caused through the activation of T cells, which initiate myelin degradation and the development of autoimmunity.
Understanding the role of Myeloid cells during MS:
Beyond the known role of T cells, MS development involves multiple mediators and cell types, including microglia and recruited macrophages. Myeloid cells contribute to the inflammatory response by releasing inflammatory cytokines, degrading the surrounding tissues and removing debris. Progressive destruction of myelin and degradation of its component proteins further fuel the autoimmune response. In the laboratory, we are trying to decipher the function of myeloid cells during the MS. We particularly interested in the phagocytic and inflammatory role of myeloid cells. We believe that targeting myeloid cells in MS patients could beneficially affect MS progression.
Increase remyelination during MS:
Chronic demyelination is a major cause of neurodegeneration in MS. However, current approved therapies for MS are aimed at shutting down the immune response in the CNS and do not address the need for remyelination. Development of therapeutic agents that would promote remyelination and prevent irreversible changes associated with neuronal death is paramount to improving the quality of life of MS patients. The CNS contains oligodendrocyte precursor cells that have the potential to differentiate into mature oligodendrocytes and remyelinate denuded axons. Although oligodendrocyte precursor cells are efficiently recruited into MS lesions, the process of axons remyelination is impaired. In the laboratory we are trying to understand the mechanisms by which remyelination is impaired during MS. We are also screening potentials drugs to enhance remyelination.