TY - JOUR
T1 - Axon Self-Destruction
T2 - New Links among SARM1, MAPKs, and NAD+ Metabolism
AU - Gerdts, Josiah
AU - Summers, Daniel W.
AU - Milbrandt, Jeffrey
AU - DiAntonio, Aaron
N1 - Funding Information:
This work was supported by NIH grant NS087632 to J.M. and A.D. and grants DA020812 and NS065053 to A.D. We thank members of the DiAntonio and Milbrandt laboratories for fruitful discussion.
Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/2/3
Y1 - 2016/2/3
N2 - Wallerian axon degeneration is a form of programmed subcellular death that promotes axon breakdown in disease and injury. Active degeneration requires SARM1 and MAP kinases, including DLK, while the NAD+ synthetic enzyme NMNAT2 prevents degeneration. New studies reveal that these pathways cooperate in a locally mediated axon destruction program, with NAD+ metabolism playing a central role. Here, we review the biology of Wallerian-type axon degeneration and discuss the most recent findings, with special emphasis on critical signaling events and their potential as therapeutic targets for axonopathy.
AB - Wallerian axon degeneration is a form of programmed subcellular death that promotes axon breakdown in disease and injury. Active degeneration requires SARM1 and MAP kinases, including DLK, while the NAD+ synthetic enzyme NMNAT2 prevents degeneration. New studies reveal that these pathways cooperate in a locally mediated axon destruction program, with NAD+ metabolism playing a central role. Here, we review the biology of Wallerian-type axon degeneration and discuss the most recent findings, with special emphasis on critical signaling events and their potential as therapeutic targets for axonopathy.
UR - http://www.scopus.com/inward/record.url?scp=84959314882&partnerID=8YFLogxK
U2 - 10.1016/j.neuron.2015.12.023
DO - 10.1016/j.neuron.2015.12.023
M3 - Review article
C2 - 26844829
AN - SCOPUS:84959314882
VL - 89
SP - 449
EP - 460
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 3
ER -