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.
Copyright © 2016 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Armadillo Domain Proteins / metabolism*
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Axons / metabolism*
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Axons / pathology*
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Cytoskeletal Proteins / metabolism*
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Humans
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Mitogen-Activated Protein Kinases / metabolism*
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NAD / metabolism*
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Neuroprotective Agents / metabolism*
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Nicotinamide-Nucleotide Adenylyltransferase / metabolism
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Signal Transduction*
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Wallerian Degeneration / metabolism*
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Wallerian Degeneration / pathology
Substances
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Armadillo Domain Proteins
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Cytoskeletal Proteins
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Neuroprotective Agents
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SARM1 protein, mouse
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NAD
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Mitogen-Activated Protein Kinases
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Nicotinamide-Nucleotide Adenylyltransferase
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Nmnat2 protein, mouse