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It is well known that primates,including humans,hardly re cover motor function after spinal cord injury (SCI) when compared with non-primate mammals such as rodents.This limited functional recovery is in part due to a non-permissive environment of the central nervous system (CNS) inhibiting axonal regrowth.This inhibitory environment for axonal regrowth is mainly caused by interaction of axon growth inhibitors with their common receptor,Nogo receptor-1 (NgR1).Axon regrowth inhibitors such as Nogo proteins,myelin associated glycoprotein (MAG),oligodendrocyte myelin glycoprotein (OMgp) and B lymphocyte stimulator (BLyS) are derived from glial cells in damaged brain.