Axonal Regeneration
The regrowth of damaged nerve cell extensions (axons). Peripheral nerves can regenerate slowly, but central nervous system axons regenerate poorly. Promoting axonal regeneration is a major unmet need. Some research peptides are investigated for potential effects on axonal regrowth in preclinical models.
Technical Context
PNS regeneration succeeds because: Schwann cells dedifferentiate after injury → clear myelin debris (with macrophages) → form bands of Büngner (aligned cellular tubes guiding regrowing axons) → produce neurotrophic factors (NGF, BDNF, GDNF) → axonal regrowth at approximately 1mm/day. CNS regeneration fails because: oligodendrocytes express inhibitory molecules (Nogo-A, MAG, OMgp binding NgR1/LINGO-1 receptor complex), reactive astrocytes form glial scar containing chondroitin sulphate proteoglycans (CSPGs, inhibiting axon growth), inflammation is poorly regulated (persistent rather than resolving), and adult CNS neurons have reduced intrinsic growth capacity (low expression of regeneration-associated genes like GAP-43). Strategies to promote CNS regeneration: blocking inhibitory molecules (anti-Nogo antibodies — in clinical trials for spinal cord injury), degrading glial scar (chondroitinase ABC), enhancing intrinsic growth (activating mTOR pathway), and providing neurotrophic support. Peptide approaches to axonal regeneration remain primarily preclinical.