Paralyzed patients may have a new treatment option, according to a recent study.
Scientists at Boston Children's Hospital and Nantong University in China studied why spinal cords that aren't completely severed stop working—and what can be done about it. In a study released Thursday in Cell, the team revealed its promising results that one day could hopefully be applied to humans.
Even when the cord isn't completely severed, many people who become paralyzed from a spinal cord injury are paralyzed from the site of the injury down. The scientists aimed to find why the nerve pathways aren't communicating and to help them start again by using paralyzed mice, but decided to approach the problem differently than previous studies.
The team wanted to find a way to approach the severed connections like a relay. "Instead of a direct flight from Boston to London, instead you have to make an indirect connection," Zhigang He, a Research Associate at Boston Children's Hospital and leader of the study, told Newsweek.
Previous animal studies often would try to get nerve fibers to regenerate. Some studies have been successful, including by this same lab, but He worries those solutions may impact the animal's motor function. Currently, patients with spinal cord injuries are treated with epidural electrical stimulation, which combines rehabilitation training with using a current on the lower spinal cord. This works for some patients, but He felt it could be better.
"The problem is if you turn off the stimulation, you don't see the function anymore," He says. "We thought if we can identify the mechanism, we might be able to do something better than electrical stimulation or combined with electrical stimulation."
The team tested multiple compounds that can alter the neuron's excitabilities and can cross the blood-brain barrier, which allows blood to the brain and spinal cord while blocking other substances. They injected the compounds into paralyzed mice for eight to 10 weeks. The most promising compound was CLP290. The mice treated with CLP290 were able to take steps after four to five weeks of treatment.
CLP290 activates a protein called KCC2, which transports chloride out of neurons. The research shows that these neurons are a key component of motor function recovery. KCC2 production declines considerably after a spinal cord injury, and then the neurons can't respond to the brain. By restoring KCC2, the neurons are able to receive signals from the brain again.
He says the team saw 80 percent of mice regain abilities like stepping and weight bearing. After many rounds of testing, the compound could be injected directly into a human patient's blood to help their injuries. The compound could also provide hope for treatment for other neuropathic disorders or epilepsy.
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