NAD+ Study Index
NAD+ (nicotinamide adenine dinucleotide) is a dinucleotide coenzyme that serves as an electron carrier in cellular redox reactions and as a substrate for sirtuin deacylases (SIRT1 through SIRT7) and PARP enzymes involved in DNA strand break repair. Intracellular NAD+ levels decline substantially with age across multiple mammalian species, a decline that correlates with impaired sirtuin activity, reduced PARP-mediated DNA repair capacity, and mitochondrial dysfunction. Research supplementing NAD+ precursors including NMN and NR in animal models has demonstrated improvements in metabolic function, muscle health, and aging-related biomarkers, with the sirtuin and mitochondrial biogenesis pathways serving as the primary proposed effectors.
Studies Listed
6
Curated Study References
Click column headers to sort. PubMed links open in a new tab where available.
| Authors ↕ | Year ↓ | Journal ↕ | Key Finding | PubMed |
|---|---|---|---|---|
| Yoshino et al. | 2021 | Science | NMN supplementation in postmenopausal prediabetic women improved skeletal muscle insulin signaling and gene expression compared to placebo, providing human clinical evidence for NAD+ precursor effects on metabolic function. | 33888596 ↗ |
| Rajman et al. | 2018 | Cell Metabolism | Comprehensive review of in vivo evidence for NAD+ precursor supplementation across aging, metabolic disease, neurodegeneration, and DNA damage models, synthesizing the mechanistic basis for sirtuin and PARP activation as primary effectors. | 29514063 ↗ |
| Imai et al. | 2013 | Cell | Review establishing the centrality of NAD+ decline to aging across species and documenting the sirtuin-mediated epigenetic, metabolic, and stress response consequences of reduced NAD+ availability in aging organisms. | 23452853 ↗ |
| Gomes et al. | 2013 | Cell | NAD+ decline in aging mice disrupted nuclear-mitochondrial communication through HIF-1alpha pseudohypoxic signaling, causing a breakdown in mitochondrial homeostasis that was reversible by NMN supplementation, directly linking NAD+ to mitochondrial aging. | 24360282 ↗ |
| Yoshino et al. | 2011 | Cell Metabolism | NMN supplementation in mouse models of diet-induced and age-induced metabolic disease restored NAD+ levels and reversed multiple metabolic dysfunction markers, providing a key preclinical study for NAD+ precursor supplementation research. | 22100409 ↗ |
| Guarente et al. | 2000 | Science | Established that Sir2 (the yeast sirtuin) requires NAD+ as a substrate and links chromatin silencing to metabolic state through NAD+/NADH ratio sensing, providing the foundational mechanistic framework for NAD+ in aging and epigenetic research. | 10930301 ↗ |
Yoshino et al.
2021, Science
NMN supplementation in postmenopausal prediabetic women improved skeletal muscle insulin signaling and gene expression compared to placebo, providing human clinical evidence for NAD+ precursor effects on metabolic function.
Rajman et al.
2018, Cell Metabolism
Comprehensive review of in vivo evidence for NAD+ precursor supplementation across aging, metabolic disease, neurodegeneration, and DNA damage models, synthesizing the mechanistic basis for sirtuin and PARP activation as primary effectors.
Imai et al.
2013, Cell
Review establishing the centrality of NAD+ decline to aging across species and documenting the sirtuin-mediated epigenetic, metabolic, and stress response consequences of reduced NAD+ availability in aging organisms.
Gomes et al.
2013, Cell
NAD+ decline in aging mice disrupted nuclear-mitochondrial communication through HIF-1alpha pseudohypoxic signaling, causing a breakdown in mitochondrial homeostasis that was reversible by NMN supplementation, directly linking NAD+ to mitochondrial aging.
Yoshino et al.
2011, Cell Metabolism
NMN supplementation in mouse models of diet-induced and age-induced metabolic disease restored NAD+ levels and reversed multiple metabolic dysfunction markers, providing a key preclinical study for NAD+ precursor supplementation research.
Guarente et al.
2000, Science
Established that Sir2 (the yeast sirtuin) requires NAD+ as a substrate and links chromatin silencing to metabolic state through NAD+/NADH ratio sensing, providing the foundational mechanistic framework for NAD+ in aging and epigenetic research.
All citations are for informational research reference purposes. Always verify directly via PubMed for current status.
Research Questions
Common questions about NAD+ research context, mechanism, and procurement.
What is NAD+ and why does it decline with age?+
What sirtuin research has been conducted linking NAD+ to aging?+
What mitochondrial research has been conducted on NAD+ supplementation?+
What human clinical research exists on NAD+ precursor supplementation?+
Related Compound Comparisons
Explore how NAD+ compares to other research compounds.
Source NAD+
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