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

Josiah Gerdts; Daniel W Summers; Jeffrey Milbrandt; Aaron DiAntonio

doi:10.1016/j.neuron.2015.12.023

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

Journal article

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

Josiah Gerdts, Daniel W Summers, Jeffrey Milbrandt and Aaron DiAntonio

Neuron (Cambridge, Mass.), Vol.89(3), pp.449-460

02/03/2016

DOI: 10.1016/j.neuron.2015.12.023

PMCID: PMC4742785

PMID: 26844829

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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.

Wallerian Degeneration - pathology

Signal Transduction

Nicotinamide-Nucleotide Adenylyltransferase - metabolism

Wallerian Degeneration - metabolism

Humans

Axons - metabolism

Neuroprotective Agents - metabolism

Animals

Axons - pathology

Armadillo Domain Proteins - metabolism

Cytoskeletal Proteins - metabolism

NAD - metabolism

Mitogen-Activated Protein Kinases - metabolism

Details

Title: Subtitle: Axon Self-Destruction: New Links among SARM1, MAPKs, and NAD+ Metabolism
Creators: Josiah Gerdts - Department of Genetics, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA
Daniel W Summers - 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
Jeffrey Milbrandt - 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
Aaron DiAntonio - 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
Resource Type: Journal article
Publication Details: Neuron (Cambridge, Mass.), Vol.89(3), pp.449-460
Publisher: United States
DOI: 10.1016/j.neuron.2015.12.023
PMID: 26844829
PMCID: PMC4742785
ISSN: 0896-6273
eISSN: 1097-4199
Grant note: NS087632 / NINDS NIH HHS R01 NS087632 / NINDS NIH HHS DA020812 / NIDA NIH HHS R01 DA020812 / NIDA NIH HHS R01 AG013730 / NIA NIH HHS NS065053 / NINDS NIH HHS R01 NS065053 / NINDS NIH HHS
Language: English
Date published: 02/03/2016
Academic Unit: Iowa Neuroscience Institute; Biology
Record Identifier: 9983991995102771

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