FIGURE 1 | Schematic representation of the CNS injury site.

Injury to the adult CNS often results in the transection of nerve fibres and damage to surrounding tissues. The distal ends of the severed axons form characteristic dystrophic growth cones that are exposed to the damaged glial environment⁴. During the early phase of injury, myelin-associated inhibitors from intact oligodendrocytes and myelin debris can restrict axon regrowth^{7, 8, 9}. Recruitment of inflammatory cells and reactive astrocytes over time leads to the formation of a glial scar, often accompanied by a fluid-filled cyst¹⁰. This scarring process is associated with the increased release of chondroitin sulphate proteoglycans, which can further limit regeneration⁴³. Together, these molecular inhibitors of the CNS glial environment present a hostile environment for axon repair.

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