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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.

NMNAT1 inhibits axon degeneration via blockade of SARM1-mediated NAD + depletion