Abstract Title:

Activation of SIRT3 by the NAD(+) Precursor Nicotinamide Riboside Protects from Noise-Induced Hearing Loss.

Abstract Source:

Cell Metab. 2014 Dec 2 ;20(6):1059-68. PMID: 25470550

Abstract Author(s):

Kevin D Brown, Sadia Maqsood, Jing-Yi Huang, Yong Pan, William Harkcom, Wei Li, Anthony Sauve, Eric Verdin, Samie R Jaffrey

Article Affiliation:

Kevin D Brown

Abstract:

Intense noise exposure causes hearing loss by inducing degeneration of spiral ganglia neurites that innervate cochlear hair cells. Nicotinamide adenine dinucleotide (NAD(+)) exhibits axon-protective effects in cultured neurons; however, its ability to block degeneration in vivo has been difficult to establish due to its poor cell permeability and serum instability. Here, we describe a strategy to increase cochlear NAD(+) levels in mice by administering nicotinamide riboside (NR), a recently described NAD(+) precursor. We find that administration of NR, even after noise exposure, prevents noise-induced hearing loss (NIHL) and spiral ganglia neurite degeneration. These effects are mediated by the NAD(+)-dependent mitochondrial sirtuin, SIRT3, since SIRT3-overexpressing mice are resistant to NIHL and SIRT3 deletion abrogates the protective effects of NR and expression of NAD(+) biosynthetic enzymes. These findings reveal that administration of NR activates a NAD(+)-SIRT3 pathway that reduces neurite degeneration caused by noise exposure.

Study Type : Animal Study

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