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.