FGF2 is among the most effective neuroprotective growth factors in diverse models of CNS injury, including stroke, trauma, excitotoxicity, and axotomy (38, 39) . In contrast to this expected protective effect of FGF2 on neurons, removal of endogenous FGF2 actually improved regenerative parameters in lesions that involved remyelination. Improved regeneration of oligodendrocytes was observed in FGF2 j/j mice after acute cuprizone demyelination of the corpus callosum and after murine hepatitis virus strain A59 demyelination of spinal cord ( [11, 12] current study). In an example from the peripheral nervous system, FGF2 knockout mice were used to prevent the normal upregulation of FGF2 and FGF receptor (FGFR) activation associated with Schwann cells and macrophages at a site of sciatic nerve crush injury (40) . Compared with wild-type mice, the FGF2 knockout mice exhibited improved myelination and increased axon diameter during regeneration from sciatic nerve crush (40) . These results indicate that a detrimental effect of endogenous FGF2 on remyelination may outweigh FGF2 protection from acute axon damage in these lesion models. Indeed, the improved remyelination in nerves of the FGF2 knockout mice may provide significant protection of axons from damage subsequent to the initial crush injury. Correlative support for a similar role of FGF2 in a chronic autoimmune model of MS can be found in a study of neural stem cell transplantation improved into mice with experimental allergic encephalomye-litis (EAE) (41) . The transplanted mice exhibited improved remyelination, with a major contribution from endogenous cells, and had less axonal loss in lesion areas. Neural stem cell transplantation was also associated with a significant decrease in FGF2 expression and reduced astroglial scar formation in the EAE lesions. FGF2 levels may modulate scar formation in demyelinated lesions because expression of FGF2 and FGFR1 corresponds with scarring, but not nonscarring, astroglial responses after other forms of CNS injury (42) .