Abstract
GAP 43 is a growth cone protein expressed in neurons especially during periods-of axonal elongation. Poor repair in the adult mammalian CNS has been ascribed to restraints upon its expression. We have cloned human GAP-43 cDNA to investigate its potential involvement in neurological illness. Analysis of postmortem human brain tissue disclosed uniformly high expression of GAP-43 throughout the neonatal brain, whereas in the adult brain high levels of GAP-43 persist only in discrete regions. However, in the wake of ischemic injury in the adult brain, regions normally low in GAP-43 reexpress it at high levels, suggesting a role for GAP-43 in remodeling and repair of mature CNS neurons.
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