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

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• 作者：Josiah Gerdts¹ ; Daniel W. Summers¹ ; ² ; Jeffrey Milbrandt¹ ; ³ ; Aaron DiAntonio² ; ³ ; ^{diantonio@wustl.edu" class="auth_mail" title="E-mail the corresponding author}
• 刊名：Neuron
• 出版年：2016
• 出版时间：3 February 2016
• 年：2016
• 卷：89
• 期：3
• 页码：449-460
• 全文大小：1333 K

文摘

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.