FRIDAY, March 20 (HealthDay News) -- A gene involved in promoting the degeneration of nerve axons in response to damage or drugs may be part of a common self-destruct program that can be targeted for the treatment of neuropathies and other conditions, according to a study published online March 15 in Nature Neuroscience.
Bradley R. Miller, and colleagues from Washington University School of Medicine in St. Louis, investigated whether dual leucine kinase (DLK) was involved in axon breakdown in fruit flies and in mice.
After severing olfactory receptor neuron axons, the researchers found that most axons degenerated in wild-type fruit flies but were significantly preserved in axons from flies lacking the fly equivalent of the DLK gene. Severing dorsal root ganglion neurons from wild-type and DLK-deficient mouse embryos or treating them with vincristine, a chemotherapeutic drug that induces axon degeneration and neuropathy, gave similar results. Severing the sciatic nerves of wild-type and DLK-deficient mice also showed that DLK deficiency significantly protected the axons, the authors report.
"Disrupting this pathway delayed axon fragmentation in response to both axotomy and the neurotoxic chemotherapeutic agent vincristine," Miller and colleagues conclude. "Thus, a common self-destruction program may promote axon breakdown in response to diverse insults and may be targetable in multiple clinical settings."
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