Nervous system protein falsely accused.

Swiss researchers have concluded that a protein accused of preventing the regeneration of nerves is innocent of the crime. This finding may eliminate one promising lead in the search for treatments for spinal cord injuries.

The adult human body has an amazing ability to repair wounds. Don't ask it to fix a severed spinal cord, however. The long nerve fibers, or axons, in the central nervous system (CNS) simply don't regenerate.

In the 1980s, investigators discovered that adult CNS axons can actually regrow if placed in the environment that normally surrounds peripheral nerves. They therefore concluded that something in the adult CNS actively prevents regeneration. Martin E. Schwab of the University of Zurich and his colleagues then found that myelin, the fatty insulation that surrounds nerves, stymies axon recovery. His group later identified a protein, IN-1, in CNS myelin that has proven to be partly responsible for this inhibition.

Last year, two other research groups suggested that they had found another important inhibitory molecule, myelin-associated glycoprotein (MAG). Schwab's team, in collaboration with a group led by Melitta Schachner of the Swiss Federal Institute of Technology in Zurich, now offers evidence that those experiments were misleading. Mice genetically manipulated not to make MAG have the same inability to regenerate damaged axons as normal mice, they report in the December 1995 Neuron.

"There is no evidence that MAG is a major inhibitor of regeneration in the CNS," says Schachner.

As a result, she adds, antibodies or other molecules that interfere with MAG are unlikely to be of much use in treating individuals paralyzed by spinal cord damage.