Multiple sclerosis is an inflammatory, demyelinating disorder that also causes neuronal dysfunction and axonal damage. Current research in the department focuses on the delineation of molecular mechanisms underlying neuronal dysfunction and axonal injury, and the role of inflammation in the modulation of such mechanisms in the spinal cord.
Ongoing research projects include:
- The role of a neuronal calcium pump, plasma membrane calcium ATPase 2 (PMCA2), in neuronal dysfunction and death in the inflamed spinal cord in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis.
- The identification of the inflammatory signals that modulate PMCA2 function in the spinal cord during EAE and in vitro.
- The contribution of astrocytes and microglia to the modulation of PMCA2-mediated neuronal dysfunction and death.
Stella Elkabes, Ph.D.
Professor & Co-Director of Reynolds Family Spine Laboratory
Department of Neurosurgery