This image represents “copolymer micelles,” tiny drug-delivery spheres that could be used in a new approach for repairing damaged nerve fibers in spinal cord injuries. The bottom graphs show data indicating damaged spinal cord tissue recovered its “action potential,” or ability to transmit signals, after treatment with the micelles. (Credit: Purdue University’s Weldon School of Biomedical Engineering)
Spinal cord injury results in immediate disruption of neuronal membranes, followed by extensive secondary neurodegenerative processes. A key approach for repairing injured spinal cord is to seal the damaged membranes at an early stage. Here, we show that axonal membranes injured by compression can be effectively repaired using self-assembled monomethoxy poly(ethylene glycol)-poly(d,l-lactic acid) di-block copolymer micelles. Injured spinal tissue incubated with micelles (60 nm diameter) showed rapid restoration of compound action potential and reduced calcium influx into axons for micelle concentrations much lower than the concentrations of polyethylene glycol, a known sealing agent for early-stage spinal cord injury. Intravenously injected micelles effectively recovered locomotor function and reduced the volume and inflammatory response of the lesion in injured rats, without any adverse effects. Our results show that copolymer micelles can interrupt the spread of primary spinal cord injury damage with minimal toxicity.
Scientists at the University of California, San Diego School of Medicine report that regeneration of central nervous system axons can be achieved in rats even when treatment delayed is more than a year after the original spinal cord injury.
Regeneration Can Be Achieved After Chronic Spinal Cord Injury
ScienceDaily (Oct. 31, 2009) — Scientists at the University of California, San Diego School of Medicine report that regeneration of central nervous system axons can be achieved in rats even when treatment delayed is more than a year after the original spinal cord injury.
“The good news is that when axons have been cut due to spinal cord injury, they can be coaxed to regenerate if a combination of treatments is applied,” said lead author Mark Tuszynski, MD, PhD, professor of neurosciences and director of the Center for Neural Repair at UC San Diego, and neurologist at the Veterans Affairs San Diego Health System. “The chronically injured axon is not dead.”
While there are more than 10,000 new spinal cord injuries annually in the United States, nearly 250,000 patients are living in the chronic stages of injury. Yet nearly all previous spinal cord injury studies have attempted to stimulate regeneration when treatment is begun almost immediately after injury — because, in part, scientists considered it very difficult to achieve regeneration at such long time points after injury. None had shown successful regeneration in the late, chronic stages.
Reporting in the October 29 issue of the Cell Press journal Neuron, the UC San Diego team demonstrated successful regeneration of adult spinal cord axons into, and then beyond, an injury site in the cervical spinal cord, the middle region of the neck. Treatment was begun at time periods ranging from six weeks to as long as 15 months after the original injury in rats.
A number of mechanisms create formidable barriers to regeneration of injured axons in chronic spinal cord injury. These include scar formation at the injury site, a partial deficiency in the intrinsic growth capacity of adult neurons, the presence of inhibitors to growth, and, sometimes, extensive inflammation. Chronically injured neurons show a loss of expression of regeneration-promoting genes, and there is progressive degeneration of spinal cord white matter beyond lesion sites — all contributing to a poor environment for axonal re-growth.
Even under ideal laboratory circumstances, axonal re-growth is complex, requiring a combination of three things: a cellular bridge in the lesion site; a nervous system growth factor to guide axons to the correct target; and a stimulus to the injured neuron that turns on regeneration genes. Using this combinatorial treatment, the research team achieved axonal bridging beyond the original lesion site in rats when treatment was delayed for up to 15 months after the original spinal cord injury. Animals lacking the full combination treatment did not exhibit axonal regrowth
3. Researchers have developed an improved version of an enzyme that degrades the dense scar tissue that forms when the central nervous system is damaged. By digesting the tissue that blocks re-growth of damaged nerves, the improved enzyme – and new system for delivering it – could facilitate recovery from serious central nervous system injuries.
The enzyme, chrondroitinase ABC (chABC), must be supplied to the damaged area for at least two weeks following injury to fully degrade scar tissue. But the enzyme functions poorly at body temperature and must therefore be repeatedly injected or infused into the body.
In a paper published November 2 in the early edition of the journal Proceedings of the National Academy of Sciences, researchers describe how they eliminated the thermal sensitivity of chABC and developed a delivery system that allowed the enzyme to be active for weeks without implanted catheters and pumps
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