Nov. 5, 2004 New Haven, Conn. -- Mice engineered without the Nogo-66 Receptor (NgR) grew new nerve fibers after spinal cord injury, pointing to this receptor as a target for development of a drug to promote fiber recovery, according to a Yale study published today in Neuron.
The researchers led by Stephen Strittmatter, M.D., professor of neurology and neurobiology at Yale School of Medicine, found that myelin fractions from the brain were not able to block the regrowth of nerve fibers in mice lacking the Nogo-66 Receptor protein. Myelin is the protective insulation surrounding nerve fibers of the central nervous system and loss of myelin interferes with the transmission of nerve signals. However, myelin also prevents fiber regeneration after injuries to the brain or spinal cord.
While brainstem neuronal populations show strong regenerative growth of fibers into the distal spinal cord when NgR is absent, not all fiber systems grow in the adult spinal cord. The long nerve fibers of the cortico-spinal tract that reach from the brain to the spinal cord to directly control movement did not regenerate in NgR mice after spinal cord injury.
Strittmatter said he and his colleagues will now look at the best pharmacological pathways to block the function of the Nogo-66 Receptor, and also examine whether the new fiber growth might somehow change the behavior of the animal or otherwise have subtle adverse effects. There is no indication yet of any side effects from blocking the receptor.
Co-authors included Ji-Eun Kim, Betty Liu, and James Park, all of Yale.
Citation: Neuron, Vol. 44, pp 1-20 (October 28, 2004)
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