| Literature DB >> 21071441 |
Yo Sasaki1, Jeffrey Milbrandt.
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.Entities:
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Year: 2010 PMID: 21071441 PMCID: PMC3009846 DOI: 10.1074/jbc.C110.193904
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157