NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and bench research with no human data
PubMed 27127236 · doi:10.1126/science.aaf2693
What was done
Researchers investigated the role of cellular oxidized nicotinamide adenine dinucleotide (NAD+) levels and mitochondrial function in muscle stem cell senescence. Aged mice and an mdx mouse model of muscular dystrophy were treated with the NAD+ precursor nicotinamide riboside. The researchers also assessed the effects of nicotinamide riboside on neural stem cells, melanocyte stem cells, and overall mouse lifespan.
What was found
The abstract reports that nicotinamide riboside induced the mitochondrial unfolded protein response and prohibitin protein synthesis, rejuvenated muscle stem cells in aged mice, and prevented muscle stem cell senescence in mdx mice. It also delayed senescence in neural and melanocyte stem cells and increased mouse lifespan. The abstract reports no numerical values, effect sizes, or survival statistics.
Why it matters
The study suggests cellular NAD+ availability serves as a switch regulating adult stem cell senescence across multiple tissue types and that NAD+ repletion can enhance regenerative capacity in aged mice.
Limits
All findings are derived from mouse models and may not generalize to humans. The abstract does not provide sample sizes, dosing details, duration of treatment, or quantitative measures of lifespan extension.
Cited by
- supports Administering nicotinamide riboside, a precursor to NAD, causes mice to gain or maintain muscle mass.