These data suggest that the enhanced tau protein phosphorylation occurs upon severe neuron injures and may contribute to the pathological structural changes of CNS leading to brain damage of TBI.

This study explored the function and possible mechanism of bone morphogenetic protein-2 (BMP-2) in the healing of injured peripheral nerves in vivo. Rabbit facial nerves were injured by clamping and then treated with recombinant human BMP-2 (rhBMP-2) or phosphate-buffered saline (control) by injecting once during surgery and twice a day post-injury for 7 days. Facial nerve fragments within 5 mm of the clamping point were examined at different times post-surgery. Axon structures visualized by Bielschowsky staining were similar in experimental and control nerves 2 and 6 weeks post-injury. At 4 weeks post-injury, cross-section images of facial nerves showed that axons treated with rhBMP-2 were denser and thicker, and levels of tau protein were increased. It is concluded from these data that rhBMP-2 may affect injured facial nerve regeneration by inducing more neurons to return to embryonic patterns of tau gene expression.