There is still no specific cure for spinal cord injury, and various treatments, including brain-machine interfaces, are under development. The axons of adult central nerves are extremely difficult to regenerate once damaged. The difficulty in recovering neural function after spinal cord injury is largely due to the inability to reform neural circuits due to this inability to regenerate axons. In this axon regeneration, chondroitin sulfate, a sulfated glycan, plays a central role as an inhibitory molecule. CS produced at the site of injury activates the receptor-type protein tyrosine phosphatase σ expressed at the cut end of the axon, causing dephosphorylation of cortactin, failure of autophagosome-lysosome fusion, and formation of dystrophic endballs downstream. As a result, axon regeneration is inhibited.