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

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.

• Authors: Yo Sasaki, Jeffrey Milbrandt
• Journal: The Journal of biological chemistry (J Biol Chem) Vol. 285 Issue 53 Pg. 41211-5 (Dec 31 2010) ISSN: 1083-351X [Electronic] United States
• PMID: 21071441 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Proteins
• Nmnat protein, mouse
• NMNAT1 protein, human
• Nicotinamide-Nucleotide Adenylyltransferase

Topics

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