The discovery of the receptor for a molecule that controls nerve growth could lead to new treatments for brain and spinal injury.
Researchers at Yale University have identified the nerve cell receptor for a protein called Nogo, which stops nerves sprouting new connections. They hope to develop new drugs to block the interaction of Nogo and its receptor, dubbed NgR. This should allow damaged nerve cells to regrow.
The discovery 鈥渙pens up many more potential types of compounds鈥� for treatments, says Steve Strittmatter, who led the research.
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Martin Schwab, a neuroscientist at the University of Zurich, and one of the discoverers of the gene for Nogo, says: 鈥淭his is the first step to understanding how neurons respond to Nogo.鈥�
But he warns: 鈥淭urning a paraplegic into someone who can move around normally is a goal that may never be within reach.鈥�
However, some quadraplegics are unable to breathe or speak unaided and returning these abilities would be a tremendous gain, he says. Restoring limited standing and walking would also combat muscle wasting and joint problems in patients.
Uncontrolled rewiring
Nerve cells connect to each other by extending long spidery branches called axons. If axons in the adult brain or spinal cord are damaged, molecules such as Nogo stop them from sprouting new connections, and they cannot grow back fully. This causes permanent disability or paralysis.
Although this has devastating consequences for patients, Strittmatter speculates that it performs an important role in healthy people. 鈥淥nce you鈥檝e built the brain correctly, you want to stop it from rearranging too much,鈥� he says.
However, he hopes that interfering with Nogo should not cause uncontrolled neuronal rewiring in patients鈥� spines or brains. Schwab鈥檚 team in Switzerland is already working on therapies to block Nogo. They have found that blocking Nogo causes controlled axonal regrowth, and only small scale related rewiring in the brain.
The Swiss team is using antibodies to block Nogo鈥檚 action. These antibodies can restore the ability to walk in rats whose spinal cords have been partially cut.
But antibodies are difficult to manufacture, and tricky to work with. Smaller proteins that could stop NgR receptors responding to Nogo would be much easier to administer, and much easier to produce on a large scale, says Strittmatter.
More at: Nature (vol 409, p 341)