Researchers at the University of Kentucky College of Medicine have identified a series of molecular signals that lead to apoptosis and further neurologic damage during the initial weeks following a spinal cord injury.
The study, published this month in Nature Medicine, shows that mitochondria of neurons damaged in spinal cord injuries release the protein cytochrome c, which causes two other proteins, apaf-1 and procaspase-9, to bind. The binding process activates the caspase-3 enzyme, which cleaves several other proteins, resulting in DNA fragmentation and destruction of the cellular structure. These signals eventually reach and trigger apoptosis in oligodendroglia cells that form myelin in the central nervous system.
"The oligodendroglia, although undamaged by the original injury, can die in the weeks following the trauma," said Pamela Knapp, PhD, assistant professor of anatomy and neurobiology and coauthor of the study.
"By developing therapeutic strategies that can prevent the death of . . . [Full Text of this Article]
