LEXINGTON, KY (July 26, 1999) - Spinal cord injuries result from damage to cells during the weeks following the injury as well as at the time of the trauma. In the August issue of Nature Medicine, University of Kentucky College of Medicine researchers report the discovery of the molecular signals that lead to apoptosis, or programmed cell death, following spinal cord injury.

"This work represents a major advancement in our understanding of how and why cells in the spinal cord die following injury," said Joe Springer, Ph.D., associate professor, Department of Anatomy and Neurobiology, UK College of Medicine, and lead author of the paper. "This study will be important in directing future research efforts, including the development of drugs to limit the consequences of spinal cord injury."

About 250,000 Americans have spinal cord injuries, and about 10,000 new cases occur each year. In Kentucky, about 1,100 people suffer from spinal cord injuries with about 200 new cases each year.

People between the ages of 16 and 30 account for more than half of all spinal cord injuries, and spinal cord injuries are three times more prevalent in males than females.

The incidence of spinal cord injuries is rare compared to other health problems, such as heart disease, cancer or stroke. However, the total financial burden of spinal cord injuries is disproportionately high. The estimated cost of spinal cord injuries in the United States was $7.7 billion in 1995, and a 27-year-old with complete quadriplegia will incur lifetime costs of about $1 million.

Apoptosis is a "suicide" process. The dying cell activates internal biochemical reactions, such as fragmentation of the DNA, to disassemble itself systematically. One cell type that undergoes apoptosis after the injury is the oligodendroglia, which provides myelin to the nerves controlling motor function. Myelin acts as an essential insulator of nerves, and wi
'"/>

Contact: Maureen McArthur
mhmcar2@pop.uky.edu
606-323-6363
University of Kentucky Medical Center
27-Jul-1999