Shuxin Li, M.D., Ph.D.
Assistant Professor of Neurology
Following central nervous system (CNS) injury, or with degenerative neurological disorders, loss of neuronal cells and axonal disconnection of surviving neurons may result in persistent dysfunction with a limited recovery. Promotion of neuronal survival and axonal regrowth are essential for injury repair in the CNS. We are interested in exploring the cellular and molecular mechanisms underlying failure of axonal regeneration and cell death in the damaged CNS. One area of our research is to characterize axonal growth inhibition mediated by extrinsic factors, such as myelin-derived molecules and glial scar-related proteoglycans, and regulated by the intracellular downstream signaling pathways. Another emphasis of our studies is to understand the intracellular signaling mechanisms underlying the neural cell death in the CNS after injury. The final goal of our research is to develop potential therapeutic strategies for improving recovery from CNS injury by stimulating axonal regeneration in surviving axotomized-neurons and by promoting the survival of injured neural cells via targeting various molecules.
Selected Publications:
Li S and Strittmatter SM. Delayed systemic Nogo-66 receptor antagonist after spinal cord injury promotes recovery. J Neurosci, 2003; 23: 4219-4227. (Highlighted paper)
Kim JK*, Li S*, GrandPre T, Qiu K, Greer CA and Strittmatter SM. Axon Regeneration in young adult mice lacking Nogo-A/B. Neuron, 2003; 38: 187. 2003. (*Co-first author)
Zheng B, .Ho C, .Li S, Keirstead H, Steward O, Tessier-Lavigne M. Lack of enhanced spinal regeneration in Nogo deficient mice. Neuron 2003; 38: 213.
GrandPré T*, Li S * and Strittmatter SM. Nogo-66 receptor antagonist peptide promotes axonal regeneration. Nature, 2002; 417: 547-551. (*Co-first author).
Li S and Stys PK. Mechanisms of ionotropic glutamate receptor-mediated excitotoxicity in isolated spinal cord white matter. J Neurosci 2000; 20: 1190-1198. (Cover Figure)
Li S, Mealing GAR, Morley P, Stys PK. Novel injury mechanism in anoxia and trauma of spinal cord white matter: glutamate release via reverse Na+-dependent glutamate transport. J Neurosci 1999; 19: RC 16(1-9). (Cover Figure)