Abstract

Overexpression of the NAD+biosynthetic enzyme NMNAT1 leads to preservation of injured axons. While increased NAD+or decreased NMN levels are thought to be critical to this process, the mechanism(s) of this axon protection remain obscure. Using steady-state and flux analysis of NAD+metabolites in healthy and injured mouse dorsal root ganglion axons, we find that rather than altering NAD+synthesis, NMNAT1 instead blocks the injury-induced, SARM1- dependent NAD+consumption that is central to axon degeneration.

Original languageEnglish
Article numbere19749
JournaleLife
Volume5
Issue numberOCTOBER2016
DOIs
StatePublished - Oct 13 2016

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