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Axonal degeneration is blocked by nicotinamide mononucleotide adenylyltransferase (Nmnat) protein transduction into transected axons.

Publication date: 2010-12-31

Journal: The Journal of Biological Chemistry

Keywords: Animals, Axons, metabolism, Cell Line, Cells, Cultured, Ganglia, Spinal, Humans, Lentivirus, Mice, Models, Biological, Models, Neurological, Neurodegenerative Diseases, Neurons, Nicotinamide-Nucleotide Adenylyltransferase, Proteins, chemistry

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Abstract

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.

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PubMed ID:: 21071441

PMC ID:: 3009846

DOI:: 10.1074/jbc.C110.193904

ScienceOpen disciplines: Chemistry

Keywords: Animals,Axons,metabolism,Cell Line,Cells, Cultured,Ganglia, Spinal,Humans,Lentivirus,Mice,Models, Biological,Models, Neurological,Neurodegenerative Diseases,Neurons,Nicotinamide-Nucleotide Adenylyltransferase,Proteins,chemistry

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ScienceOpen disciplines: Chemistry

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