According to research published in Stem Cell Reports, a spinal cord injury (SCI) can cause irreparable neurological damage if not treated promptly. Despite the lack of clarity on the therapeutic application of this method, previous research has shown that spinal GABA neurons produced from human pluripotent stem cells (hPSCs) can decrease stiffness and improve movement in rats following SCI.
Researchers describe how they created a rhesus macaque (Macaca mulatta) model of SCI by hemisecting the spinal cord at T10, which produces neuronal conduction failure and neurological dysfunction in humans, including motor deficits, pain, and spasms.
Transplanted human spinal GABA neurons lived for up to 7.5 months in the spinal cord of an injured monkey, during which time they continued to grow, expand their axons, and form connections. Only the activation of engineered receptors by designer drugs gives critical proof of their functional feasibility.
These findings represent a significant advancement in the development of spinal neuron transplantation as a therapeutic option for the treatment of SCI in people. Spinal cord injuries (SCIs) are highly damaging since the nerve cells are permanently damaged. Damaged brain circuits cannot be repaired, and new neurons cannot develop in their place, preventing functional recovery.
Recent studies into rebuilding damaged brain circuitry have focused on neural stem cells (NSCs), also known as neuronal progenitor cells (NPCs), which have the ability to develop into neurons.
Human spinal neurons are highly integrated into rat neural circuits, and current research indicates that spinal NSCs produced from human pluripotent stem cells (hPSCs) can create significant axon regeneration, aiding in the recovery of lost mobility. Nonetheless, these investigations have only looked at how excitatory glutamatergic neurons in relay networks regulate motor performance.
Pain and stiffness are frequent symptoms of spinal cord injury (SCI), affecting up to 90% and 65% of drug-refractory SCI patients, respectively, and can have a catastrophic impact on quality of life. After birth, spinal dI4 GABA neurons play a crucial role in the presynaptic modulation of sensory terminals.
These neurons also aid in the prevention of aberrant sensations, the maintenance of adequate muscular tone, and the easy gripping and movement of the forelimbs and hindlimbs. Because GABA neurons have been shown to be effective in reducing pain in rats, their possible shortage following SCI, which leads to overexcitation of sensory transmission and excitatory interneurons, may explain the subsequent pain and spasms.
However, some findings indicate that there is presently no mechanism for producing human spinal GABA neurons in vitro. Human spinal GABA neurons have been demonstrated to enhance movement, pain, and stiffness in rats suffering from spinal cord injury.
However, due to significant variations between rats and humans, demonstrating effectiveness in a rodent model does not guarantee the same outcome in humans. Before initiating clinical trials, assess the efficacy and safety of therapies in big animals or even nonhuman primates (NHPs) that are extremely comparable to humans in neuroanatomy and neurophysiology.
