Richard Borgens and his team comprising of physiologist Riyi Shi and chemist Youngnam Cho from the Center for Paralysis Research at the Purdue School of Veterinary Medicine have discovered that Chitosan, the simple sugar found in the crustacean shells of lobsters, is capable of targeting damaged membranes.
Researchers started experimenting on guinea pigs. They first isolated and compressed a segment of the rodent’s spinal cord. Subsequently, they applied the chemical and a fluorescent dye that could only enter the cells through damaged membranes. Scrutinizing the tissues under the microscope, the investigators noted that all the neurons in the spinal cord tissue remained unstained by the dye. Moreover, while measuring the guinea pigs’ brain response, they observed that the signals failed to reach the brain because of the damaged spinal cord. Thirty minutes after injecting the sugar mixed with sterile water into the bloodstream of the animals the researchers found that the damaged cells had been repaired.
The experts stated, “However, 30•min after injecting chitosan into the rodents, the signals miraculously returned to the animals’ brains.” Researchers theorize that the injected sugar migrates to the spinal cord injury where it plugs holes in the coating of the nerve cells.
Borgens added, “Science has moved in a new direction. Previously we have been looking at drugs which would potentially reduce damage. Now we are looking at complete repair.”
2. Rats with damaged spines can walk again thanks to acupuncture. The ancient treatment seems to stop nerve cell death by reducing inflammation. A clinical trial has begun Trials show that it improves sensory and motor functions in people with spinal cord injuries. The acupuncture treatment on the rats was given almost immediately after injury, but most patients don’t seek acupuncture until at least three months after damage to their spines.
3. Researchers found that by immediately giving injured rats a drug that acts on a specific gene, they could halt the dangerous bleeding that occurs at the site of spinal damage.
In the study, Simard and his colleagues gave a drug called antisense oligodeoxynucleotide (ODN) to rodents with spinal cord injuries for 24 hours after the injury occurred. ODN is a specific single strand of DNA that temporarily blocks genes from being activated. In this case, the drug suppresses the Sur1 protein, which is activated by the Abcc8 gene after injury.
After routine injuries, Sur1 is usually a beneficial part of the body’s defense mechanism, preventing cell death due to an influx of calcium, the researchers explained. However, in the case of spinal cord injury, this defense mechanism goes awry. As Sur1 attempts to prevent an influx of calcium into cells, it allows sodium in, Simard explained, and too much sodium can cause the cells to swell, blow up and die.
The new gene-targeted therapy might put a stop to that. Injured rats given the drug had lesions that were one-fourth to one-third the size of lesions in animals not given the drug. The animals also recovered from their injuries much better.