Study summary · research use only
NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this mouse study, the amount of oxidized nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity were examined as a factor in muscle stem cell (MuSC) senescence during aging. Treatment with the NAD+ precursor nicotinamide riboside (NR) was reported to induce the mitochondrial unfolded protein response and prohibitin protein synthesis, and was associated with rejuvenation of MuSCs in aged mice. NR was also reported to prevent MuSC senescence in the mdx (C57BL/10ScSn-Dmd(mdx)/J) mouse model of muscular dystrophy, to delay senescence of neural stem cells and melanocyte stem cells, and to increase mouse life span. The authors state that strategies conserving cellular NAD+ may reprogram dysfunctional stem cells and improve life span in mammals.
Abstract
Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD(+)) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD(+) precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmd(mdx)/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD(+) may reprogram dysfunctional SCs and improve life span in mammals.
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