Human spinal GABA neurons survive and mature in the injured nonhuman primate spinal cord

Spinal cord injury (SCI) leads to permanent neural dysfunction without effective therapies. We previously showed that human plurip-otent stem cell (hPSC)-derived spinal GABA neurons can alleviate spasticity and promote locomotion in rats after SCI, but whether this strategy can be translated into the clinic remains elusive. Here, a nonhuman primate (NHP) model of SCI was established in rhesus macaques (Macaca mulatta) in which the T10 spinal cord was hemisected, resulting in neural conduction failure and neural dysfunction, including locomotion deficits, pain, and spasms. Grafted human spinal GABA neurons survived for up to 7.5 months in the injured monkey spinal cord and retained their intrinsic properties, becoming mature and growing axons and forming synapses. Importantly, they are functionally alive, as evidenced by designer receptors exclusively activated by designer drug (DREADD) activation. These findings represent a significant step toward the clinical translation of human spinal neuron transplantation for treating SCI.

Automated summary

The researchers established a model of spinal cord injury in rhesus macaques and found that transplanted human spinal GABA neurons survived and showed functional activity in the injured monkey spinal cord, indicating a significant step toward clinical translation for treating spinal cord injury.