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Ed. Note: The following
is a press release from Yale University.
Oct. 27, 2004 -- 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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