nicotinamide-beta-riboside and Muscular-Dystrophies

nicotinamide-beta-riboside has been researched along with Muscular-Dystrophies* in 1 studies

Other Studies

1 other study(ies) available for nicotinamide-beta-riboside and Muscular-Dystrophies

Article	Year
NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice. Science (New York, N.Y.), 2016, Jun-17, Volume: 352, Issue:6292 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. Topics: Animals; Cellular Reprogramming; Cellular Senescence; Disease Models, Animal; Longevity; Melanocytes; Mice; Mice, Inbred C57BL; Mice, Inbred mdx; Mitochondria; Muscular Dystrophies; Myoblasts, Skeletal; NAD; Neural Stem Cells; Niacinamide; Oxidative Stress; Prohibitins; Pyridinium Compounds; Repressor Proteins; Unfolded Protein Response	2016

Article

Year

NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice.

Science (New York, N.Y.), 2016, Jun-17, Volume: 352, Issue:6292

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.

Topics: Animals; Cellular Reprogramming; Cellular Senescence; Disease Models, Animal; Longevity; Melanocytes; Mice; Mice, Inbred C57BL; Mice, Inbred mdx; Mitochondria; Muscular Dystrophies; Myoblasts, Skeletal; NAD; Neural Stem Cells; Niacinamide; Oxidative Stress; Prohibitins; Pyridinium Compounds; Repressor Proteins; Unfolded Protein Response

2016