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One of goals of treatment in injuries to the nervous system and in diseases like multiple sclerosis is to limit nerve damage. A study of spinal cord injury in mice has found a mechanism that might provide the answer. One of the holy grails in injuries to the nervous system and even in diseases like multiple sclerosis, Parkinson's and Alzheimer's is to limit the damage spreading and encourage healing. Nerve cells take offence very easily and can turn up their toes even though they weren't harmed themselves. One of the reasons is that a natural phenomenon occurs abnormally in the injured brain and spinal cord. It's called programmed cell death and is a vital part of human survival. Without it we'd develop cancer even more frequently than we do and embryos wouldn't turn into properly formed fetuses because programmed cell death stops uncontrolled cell division and allows tissues to be carved into shape. Anyway, a study of spinal cord injury in mice has found a lock and key mechanism - a receptor - which seems to fire off this abnormal cell death in damaged spinal cord. And when the scientists blocked this receptor, the mice recovered far more function than their fellows left unblocked. The challenge is to see whether this applies to humans, say after an acute spinal injury or whether a cocktail of treatments might be needed. Because one concern over fiddling with programmed cell death is that a side effect could be cancer.
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