IDENTIFYING AND PREVENTING THE INTRICATE INJURY MECHANISMS
THAT OCCUR IMMEDIATELY AFTER SCI
W. Dalton Dietrich, PhD • John R. Bethea, PhD • Robert P. Yezierski, PhD

An active area of research at the Miami Project is in developing neuroprotective treatments to protect the spinal cord in the first hours and days after the injury. There is a belief that limiting the degree of secondary injury will limit the severity of neurological deficits after SCI and may therefore enhance the recovery of function.

Many studies provide evidence that apoptosis, an active cell-suicide program, is responsible for some cell death following SCI. Very little information is available about anti-apoptotic mechanisms that inhibit programmed cell death within the injured spinal cord. Data from John Bethea, PhD and W. Dalton Dietrich, PhD indicate that inhibitors of apoptosis do exist within the spinal cord cells which may help them survive. By gaining a better understanding of these intricate molecular, cellular, and regulatory events that occur following SCI, we may be able to design new therapeutic strategies to enhance natural healing mechanisms and to diminish those events that lead to further damage.

Systemic modest hypothermia may be one such therapy. When modest systemic hypothermia was induced following SCI in rodents, the total area of spinal cord damage was reduced. The researchers, including Dr. Robert Yezierski (now at the University of Florida), also found that the hypothermia-treated rodents had preserved locomotor function. While further research is required to determine the mechanism by which hypothermia exerts its neuroprotective effect, the results suggest that this intervention is a promising strategy in treating acute SCI.