Promoting axon regneration and functional recovery after spinal cord injury

Boston Children'S Hospital, Boston MA

Investigators

Linked publications & trials

Abstract

Spinal cord injury disrupts the connections between the brain and spinal cord, often resulting in the loss of sensory and motor function below the lesion site. The most important reason for such permanent functional deficits is the failure of injured axons to regenerate after injury. In principle, the functional recovery could be achieved by two forms of axonal regrowth: the regeneration of lesioned axons which will reconnect with their original targets and the sprouting of spared axons that form new circuits and compensate for the lost function. Our recent studies reveal the activity of the mammalian target of rapamycin (mTOR) pathway, a major regulator of new protein synthesis, as a critical determinant of axon regrowth in the adult retinal ganglion neurons. This proposed study will focus on examining the possibility of whether manipulating the mTOR activity could promote the regrowth of descending corticospinal axons and restoration of lost functions after spinal cord injury. We expect that these experiments will provide important insights into the therapeutic potential of manipulating mTOR pathway in promoting axon regrowth and functional recovery after spinal cord injury.