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5 December 2013 11:26 am ,
Vol. 342 ,
An animal rights group known as the Nonhuman Rights Project filed lawsuits in three New York courts this week in an...
Researchers have been hot on the trail of the elusive Denisovans, a type of ancient human known only by their DNA and...
Thousands of scientists in the Russian Academy of Sciences (RAS) are about to lose their jobs as a result of the...
Dyslexia, a learning disability that hinders reading, hasn't been associated with deficits in vision, hearing, or...
Exotic, elusive, and dangerous, snakes have fascinated humankind for millennia. They can be hard to find, yet their...
Researchers have sequenced and analyzed the first two snake genomes, which represent two evolutionary extremes. The...
Snake venoms are remarkably complex mixtures that can stun or kill prey within minutes. But more and more researchers...
At age 30, Dutch biologist Freek Vonk has built up a respectable career as a snake scientist. But in his home country,...
- 5 December 2013 11:26 am , Vol. 342 , #6163
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Brake on Nerve Repair Identified
18 January 2001 7:00 pm
Unlike skin cells, neurons in the brain and spinal cord don't grow back after they've been injured. This intransigence seems to crop up as soon as developing neurons grow their insulating sheath made of myelin. Last year, scientists found the gene for a protein in myelin that shut down nerve growth. But they had no idea how this protein signal, called Nogo, gets picked up.
To find out, a team led by Stephen Strittmatter of Yale University sampled genes expressed in mouse brain to look for ones that would allow nonneuronal cells to bind Nogo (which they normally wouldn't do). They found their needle in a haystack: a gene they named NgR. Another experiment bolstered the idea that NgR is a Nogo receptor: When young neurons were manipulated to produce the NgR protein, they stopped growing in the presence of Nogo, the team reports in the 18 January issue of Nature.
The finding gives researchers "a very strong handle" on how Nogo stops nerve growth, says Marie Filbin of Hunter College of the City University of New York. Buoyed by this understanding, Strittmatter hopes that injured neurons could be encouraged to regrow, perhaps with a small molecule or peptide to disrupt the partnering of Nogo with its receptor. Such a treatment may eventually help people with spinal cord injuries. But just blocking only NgR may not be enough, cautions Filbin, who thinks that other signals besides Nogo may block regrowth.