Current Opinion in Chemical Biology | VOL. 69
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The chemical biology of NAD+ regulation in axon degeneration

Publication Date Aug 1, 2022

Abstract

During axon degeneration, NAD+ levels are largely controlled by two enzymes: nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) and sterile alpha and toll interleukin motif containing protein 1 (SARM1). NMNAT2, which catalyzes the formation of NAD+ from NMN and ATP, is actively degraded leading to decreased NAD+ levels. SARM1 activity further decreases the concentration of NAD+ by catalyzing its hydrolysis to form nicotinamide and a mixture of ADPR and cADPR. Notably, SARM1 knockout mice show decreased neurodegeneration in animal models of axon degeneration, highlighting the therapeutic potential of targeting this novel NAD+ hydrolase. This review discusses recent advances in the SARM1 field, including SARM1 structure, regulation, and catalysis as well as the identification of the first SARM1 inhibitors.

Concepts

Nicotinamide Mononucleotide Adenylyltransferase 2 Neurodegeneration In Animal Models Axon Degeneration SARM1 Activity Sterile Alpha Sterile Alpha Motif Models Of Degeneration Concentration Of NAD Toll Interleukin Nicotinamide Mononucleotide

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