Delayed inhibition of Nogo-A does not alter injury-induced axonal sprouting but enhances recovery of cognitive function following experimental traumatic brain injury in rats.

@article{Lenzlinger2005DelayedIO,
  title={Delayed inhibition of Nogo-A does not alter injury-induced axonal sprouting but enhances recovery of cognitive function following experimental traumatic brain injury in rats.},
  author={Philipp M. Lenzlinger and Shunichi Shimizu and Niklas Marklund and Hilaire J Thompson and Martin E. Schwab and Kathryn E. Saatman and Rachel C Hoover and Florence Martine Bareyre and Melissa Motta and Amy Luginbuhl and Regina Pape and Angela K Clouse and Cristina M Morganti-Kossmann and T K Mcintosh},
  journal={Neuroscience},
  year={2005},
  volume={134 3},
  pages={1047-56}
}
Traumatic brain injury causes long-term neurological motor and cognitive deficits, often with limited recovery. The inability of CNS axons to regenerate following traumatic brain injury may be due, in part, to inhibitory molecules associated with myelin. One of these myelin-associated proteins, Nogo-A, inhibits neurite outgrowth in vitro, and inhibition of Nogo-A in vivo enhances axonal outgrowth and sprouting and improves outcome following experimental CNS insults. However, the involvement of… CONTINUE READING
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