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Neurons in the peripheral nervous system (PNS) have the capability to regenerate after injury or disease while central nervous system (CNS) neurons do not. Elucidation of the reasons for this difference in regenerative ability is crucial to developing treatments for sufferers of CNS disorders, injury, and stroke. Therefore, my lab investigates molecular mechanisms underlying neuronal repair, axonal guidance, and growth cone formation and collapse. We discovered the Nogo protein and its inhibitory role in CNS repair. The Nogo protein interacts with the Nogo-66 receptor (NgR), located on the axons of CNS neurons, to inhibit axonal sprouting after injury. Blockage of this interaction by a competitive inhibitor allows limited CNS axon regeneration in vitro and in spinal cord injury model mice. During normal development and repair, axonal pathfinding is mediated by the growth cone, which is guided by extra cellular cues that repel or attract the extending axon. This extension is the result of continuous polymerization and depolymerization of the actin skeleton. My lab works to elucidate the mechanism behind how these growth cones are guided, and we have uncovered a number of important steps in this pathway. Understanding the inhibitory environment to CNS regeneration is essential to developing treatments for its disorders.

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