Axonal degeneration is blocked by nicotinamide mononucleotide adenylyltransferase (Nmnat) protein transduction into transected axons.
Axonal degeneration is an early and important component of many neurological disorders. Overexpression of nicotinamide mononucleotide adenylyltransferase (Nmnat), a component of the slow Wallerian degeneration (Wld(s)) protein, protects axons from a variety of insults. We found that transduction of Nmnat protein into severed axons via virus-like particles prevented axonal degeneration. The post-injury efficacy of Nmnat indicates that its protective effects occur locally within the axon and provides an opportunity to develop novel agents to treat axonal damage.
Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63110, USA.
Yo
Y
Sasaki
Jeffrey
J
Milbrandt
D000818:Animals; D001369:Axons / Q000378:metabolism*; D002460:Cell Line; D002478:Cells, Cultured; D005727:Ganglia, Spinal / Q000378:metabolism*; D006801:Humans; D016086:Lentivirus / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D008959:Models, Neurological; D019636:Neurodegenerative Diseases; D009474:Neurons / Q000378:metabolism; D009612:Nicotinamide-Nucleotide Adenylyltransferase / Q000378:metabolism*; D011506:Proteins / Q000737:chemistry
D009612:Nicotinamide-Nucleotide Adenylyltransferase; D011506:Proteins; C484007:NMNAT1 protein, human; C510972:Nmnat1 protein, mouse