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 - 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
SN - 0896-6273
VL - 89
SP - 449
EP - 460
JO - Neuron
JF - Neuron
IS - 3
ER -