Researchers at Georgetown University Medical Center (GUMC) have been able to speed recovery and substantially reduce damage resulting from spinal cord injury in preclinical studies.
Their research, published online in Annals of Neurology and led by Kimberly Byrnes, PhD, shows that inflammation following injury causes the neurotoxicity that leads to lasting nerve cell damage, and that an experimental agent is able to block this inflammatory reaction.
"The findings we have made in this study may potentially be applicable to other neurological disorders, including stroke, head injury, Alzheimer's disease and Parkinson's disease," says senior investigator Alan I. Faden, MD, a professor of neuroscience and director of the Laboratory for the Study of Central Nervous System Injury at GUMC.
Faden says that the experimental agent they tested (CHPG), an activator of a type of glutamate receptor, is not ideal for human use because it cannot easily penetrate the blood-brain barrier. But he adds, "now that we know the biological target, a new drug could be designed that is better suited for clinical treatment of these neurodegenerative disorders."
CHPG shuts down activation of key immune cells in the brain known as microglia, which sense pathogens or damage in the spinal cord and brain. They helpfully foster the destruction of microbial invaders and clean up biological detritus that occurs after an injury, but researchers say they have a dark side as well – they can worsen the damage by releasing toxic inflammatory factors.
"Under certain conditions, like spinal cord injury and brain trauma, microglia become activated," Faden says. "They release toxic chemicals that can kill healthy adjacent tissue, and this process can continue for months.