Format

Send to

Choose Destination
Neuron. 2016 Feb 3;89(3):449-60. doi: 10.1016/j.neuron.2015.12.023.

Axon Self-Destruction: New Links among SARM1, MAPKs, and NAD+ Metabolism.

Author information

1
Department of Genetics, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA.
2
Department of Genetics, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA; Department of Developmental Biology, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA.
3
Department of Genetics, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA.
4
Department of Developmental Biology, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA. Electronic address: diantonio@wustl.edu.

Abstract

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.

PMID:
26844829
PMCID:
PMC4742785
DOI:
10.1016/j.neuron.2015.12.023
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center