NMNAT1 inhibits axon degeneration via blockade of SARM1-mediated NAD+ depletion
Dorsal root ganglion
DOI:
10.7554/elife.19749
Publication Date:
2016-10-13T11:02:13Z
AUTHORS (5)
ABSTRACT
Overexpression of the NAD+ biosynthetic enzyme NMNAT1 leads to preservation injured axons. While increased or decreased NMN levels are thought be critical this process, mechanism(s) axon protection remain obscure. Using steady-state and flux analysis metabolites in healthy mouse dorsal root ganglion axons, we find that rather than altering synthesis, instead blocks injury-induced, SARM1-dependent consumption is central degeneration.
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