NAD+ metabolism and ageing
Reviews have examined the factors that regulate NAD+ levels, the age-related decline observed in model organisms, and the roles of sirtuins, PARPs and CD38 in cellular processes1,2,3.
Research Peptide · For laboratory research use only
NAD+
Also known as Nicotinamide Adenine Dinucleotide
- Formula
- C21H27N7O14P2
- CAS
- 53-84-9
Overview
Nicotinamide adenine dinucleotide (NAD+, also nadide or beta-NAD) is a coenzyme found in all living cells. It carries electrons in reduction-oxidation reactions and is a co-substrate for non-redox enzymes, including the sirtuins, poly(ADP-ribose) polymerases (PARPs) and CD381,2,3.
Reviews describe a decline in tissue and cellular NAD+ levels with age in several model organisms and summarise research on how NAD+ synthesis and consumption are regulated1,2,3. Studies in rodents have examined raising NAD+ levels in ageing mice and the effects of NAD+ itself in brain ischaemia models4,5,6.
Mechanism of action
As described in the research literature
As described in the research literature, NAD+ links energy metabolism with signalling through NAD+-consuming enzymes. Biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) and SIRT1 activity have been described as acting together to regulate metabolism and circadian rhythm2. NAD+ is reported to influence DNA repair, chromatin remodelling, cellular senescence and immune cell function3.
In ageing mice, a decline in nuclear NAD+ was associated with accumulation of HIF-1-alpha under normoxic conditions and a specific loss of mitochondrially encoded oxidative phosphorylation subunits; raising NAD+ levels in old mice restored mitochondrial function in a SIRT1-dependent manner4. In brain ischaemia models, excessive PARP-1 activation is proposed to cause cell death by depleting intracellular NAD+, which provided the rationale for administering NAD+5,6.
Research areas
What published studies have examined
Mitochondrial communication
A study in mice examined how declining nuclear NAD+ disrupts nuclear-mitochondrial communication through a PGC-1alpha/beta-independent pathway, the effect of SIRT1 deletion, and the effect of raising NAD+ levels in old mice4.
Sources [4]
Brain ischaemia models
In a rat model of transient focal ischaemia, NAD+ was examined for its effect on brain NAD+ content, infarct formation and neurological deficits, with nicotinamide as a comparator5. A mouse model of transient middle cerebral artery occlusion examined NAD+ and its relationship to ischaemia-induced autophagy6.
Specifications
- Molecular formula
- C21H27N7O14P2
- Molecular weight
- 663.4 g/mol
- CAS number
- 53-84-9
Vial
- Form
- White to pale yellow powder in a sealed vial (500 mg or 1000 mg)
- Storage
- Store lyophilised powder at -20 °C, protected from light and moisture. Once reconstituted, keep refrigerated at 2 to 8 °C and protect from light.
- Solubility and reconstitution
- Reconstitute with bacteriostatic water. Add the diluent slowly down the inside wall of the vial and swirl gently until clear; do not shake.
Mist Applicator
- Form
- 500 mg in a vial fitted with a 10 mL mist applicator
- Storage
- Store as directed on the product label, protected from light.
- Solubility and reconstitution
- Prepare and use as directed on the product label.
References
- 1
NAD⁺ in aging, metabolism, and neurodegeneration.
Verdin E Science, 2015.
- 2
NAD+ and sirtuins in aging and disease.
Imai S, Guarente L Trends in Cell Biology, 2014.
- 3
NAD(+) metabolism and its roles in cellular processes during ageing.
Covarrubias AJ, Perrone R, Grozio A, et al. Nature Reviews Molecular Cell Biology, 2021.
- 4
Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging.
Gomes AP, Price NL, Ling AJ, et al. Cell, 2013.
- 5
Intranasal administration with NAD+ profoundly decreases brain injury in a rat model of transient focal ischemia.
Ying W, Wei G, Wang D, et al. Frontiers in Bioscience, 2007.
- 6
NAD(+) administration decreases ischemic brain damage partially by blocking autophagy in a mouse model of brain ischemia.
Zheng C, Han J, Xia W, et al. Neuroscience Letters, 2012.
This page is provided for research and educational reference only. It does not constitute medical advice, dosing guidance, or a recommendation for use. All compounds are strictly for laboratory and in-vitro research purposes.