12:12 09 April 2002
NewScientist.com news service
Chemicals that block a signal that prevents damaged nerve cells re-growing have been identified by US scientists.
The compounds stimulated the regeneration of isolated damaged rat neurons in the laboratory - and the researchers hope they might be used to help treat spinal cord injury and contribute to a better understanding of multiple sclerosis in people.
Neurons are sheathed in myelin - a fatty substance that insulates electrical signals passing along the axon. But when a neuron is damaged, myelin sends chemical signals that prevent it regenerating.
One of the three previously identified signalling pathways involves an interaction between myelin-associated glycoprotein (MAG), on the inner surface of the myelin sheath, and lipids called gangliosides on the outer surface of the axons.
A team led by Ronald Schnaar at Johns Hopkins University in Baltimore has now pinpointed four ways of blocking this pathway. These include using an antibody to prevent gangliosides bonding with MAG, and an enzyme called neuroaminidase, which prevents the interaction by destroying a critical part of the gangliosides.
Other teams have succeeded in over-riding the two other known myelin pathways that block axon re-growth. But each single method triggers only limited regeneration. Schnaar hopes that a combined treatment might be more effective. Ben Barres, a neurobiologist at Stanford University, California, agrees: "All of these three steps are very important."
Schnaar cautions that spinal cord injuries are "profoundly complex. It's still unclear what's going to be required to get functional recovery in human nerve injuries," he says.
But he hopes his research could also contribute to new treatments for multiple sclerosis. The disease involves a progressive loss of myelin around neurons. But researchers think degeneration of the axons themselves, as well as myelin degradation, could also contribute to the symptoms.
Schnaar presented his research at a meeting of the American Chemical
Society in Orlando, Florida.
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