Inflammation occurs in many disorders of the central nervous system (CNS) and it can be both beneficial and detrimental to axonal integrity and neuronal survival. Although several types of cells are involved in inflammatory responses in the CNS, activation of microglial cells is critical for this process. Microglial cells are the only endogenous immunocompetent cells in the CNS and are responsible for innate immune responses.

In this laboratory we study the role of neuroinflammation in the pathogenesis of experimental allergic encephalomyelitis (EAE), an animal model of MS. Multiple sclerosis has historically been defined as an autoimmune disease exhibiting demyelination in response to an immune attack on self myelin antigens. More recently, however, it has been increasingly recognized that there is also a neurodegenerative component and that axonal damage or loss is responsible for irreversible disability in MS patients. At present, it is generally accepted that successful treatment of MS must target both the inflammatory and neurodegenerative aspect of the disease.

In our research we employ several models of mouse and rat EAE to investigate the inflammatory and neurodegenerative mechanisms in different phases of the disease. We also use primary cell culture to study interactions between microglia and neurons, and to assess the effects of anti-inflammatory and neuroprotective drugs on these cells. Our overall goal is to develop new therapeutic strategies for MS treatment and other myelin disorders of the CNS.