January 27, 2009
Gene Could Repair Injured Nerves
Scientists identified a gene in worms that could someday lead to new therapies to repair injured or damaged nerve cells.
Researchers at the University of Utah said the gene is essential for damaged nerve cells to regenerate. By over-activating the gene, they were able to stimulate nerve regeneration much quicker than expected, even in older worms. Nerve cells have the ability to regenerate in the embryo, but lose the ability as an organism ages, researchers said. Most adult nerve cells regenerate poorly or not at all, so finding a therapy that could change that could have significant implications.
"We discovered a molecular target for a future drug that could vastly improve the ability of a neuron to regenerate after injury [either from trauma or disease]," biology professor Michael Bastiani, the leader of the research team and a member of the Brain Institute at the University of Utah was quoted as saying.
The researchers said their discovery could one day lead to ways to treat spinal cord injuries and multiple sclerosis.
For the study, scientists used nematode worms, which have molecules that perform similar functions as those in humans. The authors said their next step is to test this gene in other animals and eventually humans to see if it plays the same role.
The study focused on the gene dlk-1. When the Utah scientists over-expressed it -- making it more active than normal -- broken nerves in the worms regenerated much more quickly than expected. When dlk-1 was blocked, regeneration did not occur, scientists said.
Although the scientists believe their discovery is potentially promising, they cautioned that they also found one impediment. To trigger the regeneration, they dlk-1 protein had to act around the time of injury.
"This might be a real problem because, as a drug target, there might be a time window in which you have to activate this pathway to stimulate regeneration after a spinal cord injury," Bastiani said.
SOURCE: Science Express, published online on January 22, 2009
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