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NAD+ Peptide

NAD+ is an acronym for Nicotinamide Adenine Dinucleotide, which is considered to be an essential endogenous nucleotide, regulating primary functions such as metabolism, energy production and DNA repair. It is also considered to act as a secondary messenger via calcium dependent signaling mechanisms, possibly also serving as an immunoregulatory component (2).

NAD+ is considered by researchers to be naturally synthesized via de novo mechanism of converting the amino acid tryptophan through several enzymatic steps. Researchers posit that there are five components to NAD+ synthesis, including tryptophan, nicotinamide, nicotinic acid, nicotinamide riboside and nicotinamide mononucleotide (3).

Once synthesized, research suggests it exerts over 500 enzymatic reactions and cellular processes (12) to aid metabolic activities. Essentially, it is suggested to act as a coenzyme in redox functions, being converted to NADH, which may then involve other metabolic pathways (3).


Nicotinamide Adenine Dinucleotide (NAD+) has been suggested by researchers to act as a coenzyme, with three major classes of enzymes including: (A) deacetylase enzymes in the sirtuin class (SIRTs), (B) poly ADP ribose polymerase (PARPs) enzymes, and (C) cyclic ADP ribose synthetase (cADPRS). Research suggests that each class of enzymes interact with NAD+ in the following possible respects:

  • (A) SIRTs may stimulate mitochondrial homeostasis, stem cell regeneration, and loss of stem cells and nerve degeneration.
  • (B) PARPs, composed of 17 different enzymes, may act alongside NAD+ enzymes and synthesize poly ADP ribose polymers which may lead to genome stability.
  • (C) cADPRS include CD38 and CD157, which are considered to be key immunological cells. cADPRS appear to hydrolyze NAD+ and thereby may stimulate stem cell regeneration and DNA repair, which may be important for maintaining cellular health.

The above mentioned are suggested by researchers to be NAD+ dependent enzymes, which possibly exert their action based on Nicotinamide Adenine Dinucleotide presence. Researchers suggest that should all above three enzymes dependent on NAD+, they may compete amongst themselves for the bioavailability. It has been posited that potential function of SIRTs, for instance, may lead to reduced PARPs activity and thereby potentially lead to weakened systems. Hence, it may be critical to maintaining balance between the availability and consumption of NAD+ to obtain optimal potential impact (5).

Research and Clinical studies

NAD+ Peptide and Productive Aging

Researchers suggest that NAD+ has two key intermediates, namely nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Studies have indicated that both these intermediates may be potent agents of promoting ‘productive aging’. In a study (7), normal aging mice were presented with the NMN intermediate for 12 months. Following the study, the researchers suggested that NMN appeared to promote NAD+ synthesis in the mice that led to reduced weight gain, increased energy metabolism, enhanced physical activity, improved lipid profile and other physiological impacts.


NAD+ Peptide and Neurodegenerative Activity

Scientists consider mitochondrial dysfunction to lead to various functional limitations in electron transport chain and ATP synthesis, possibly resulting in various neurodegenerative diseases. A study (8) was conducted where aged mice were presented with NMN, NAD+ intermediate, for 3 to 12 months. The main aim of the study was to evaluate the potential impact of the peptide on mitochondrial respiratory processes, for which fluorescent NMN protein was presented to the mice models. After peptide presentation, the mitochondrial oxygen consumption rates in the nerve and brain cells of the mice were studied. Upon analysis, it was suggested that mitochondrial functions had been restored in the aged mice, suggesting that NMN may be immediately utilized by the cells to produce NAD+ and thereby exerting possible positive impact.


NAD+ Peptide and DNA Repair After Ischemic Stress

The main aim of this study (11) was to determine the neuroprotective potential of Nicotinamide Adenine Dinucleotide against ischemic stress-induced in mice. For the purpose of this study, ischemic stress was induced in the neuronal cultures in rats via deprivation of oxygen and glucose for about 2 hours. NAD+ was directly replenished into the culture medium either before or after the induced ischemic stress. After 72 hours of introducing NAD+ into the cultures, it was reported by the researchers that the DNA base excision repair activity (DNA BER), cell viability and oxidative DNA damage repair appeared to be significantly improved, irrespective of whether Nicotinamide Adenine Dinucleotide was added before or after inducing the ischemic stress.


NAD+ Peptide and the Liver, Kidney

Upon presented mice with the NAD+ peptide and stimulating increase in Nicotinamide Adenine Dinucleotide levels up to normal concentrations, researchers suggested the peptide exhibited positive potential in preventing obesity and alcoholic hepatitis, while possibly improving glucose homeostasis and overall liver health.

When aged mice kidney cells were supplemented with NAD+, the results inducated that the addition of the peptide possibly promoted SIRTs activity, which exhibited neuroprotective potential against glucose-induced kidney cell hypertrophy. Furthermore, when presented with NMN, NAD+ intermediate, it appeared to promote neuroprotective impact against cisplatin-induced kidney injury.


NAD+ Peptide and Skeletal Function

Upon presented aged mice with NMN daily for 7 days, researchers suggested that the peptide possibly led to increased ATP (energy) production, reduced inflammation and elevated mitochondrial functions.


NAD+ Peptide and Cardiac Functions

Nicotinamide Adenine Dinucleotide deficiency has been suggested by researchers to lead to reduced SIRT activity, which may cause reduced energy production and aortic constriction. When mice were presented with NMN 30 minutes before their ischemia, it reportedly produced a cardioprotective function against ischemic injury.


1. Schultz, Michael B, and David A Sinclair. “Why NAD(+) Declines during Aging: It’s Destroyed.” Cell metabolism vol. 23,6 (2016): 965-966. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5088772/

2. Braidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis. Exp Gerontol. 2020 Apr;132:110831. doi: 10.1016/j.exger.2020.110831. https://pubmed.ncbi.nlm.nih.gov/31917996/

3. Johnson, Sean, and Shin-Ichiro Imai. “NAD + biosynthesis, aging, and disease.” F1000Research vol. 7 132. 1 Feb 2018. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5795269/

4. Bieganowski P, Brenner C. Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans. Cell. 2004 May 14;117(4):495-502. https://pubmed.ncbi.nlm.nih.gov/15137942/

5. Fang, E. F., Lautrup, S., Hou, Y., Demarest, T. G., Croteau, D. L., Mattson, M. P., & Bohr, V. A. (2017). NAD+ in Aging: Molecular Mechanisms and Translational Implications. Trends in molecular medicine, 23(10), 899–916. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7494058/

6. Harden, A; Young, WJ (24 October 1906). “The alcoholic ferment of yeast-juice Part II.–The coferment of yeast-juice”. Proceedings of the Royal Society of London. Series B, Containing Papers of a Biological Character. 78 (526): 369–375. https://royalsocietypublishing.org/doi/10.1098/rspb.1906.0070

7. Mills KF, Yoshida S, Stein LR, Grozio A, Kubota S, Sasaki Y, Redpath P, Migaud ME, Apte RS, Uchida K, Yoshino J, Imai SI. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016 Dec 13;24(6):795-806. https://pubmed.ncbi.nlm.nih.gov/28068222/

8. Long AN, Owens K, Schlappal AE, Kristian T, Fishman PS, Schuh RA. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model. BMC Neurol. 2015 Mar 1;15:19. https://pubmed.ncbi.nlm.nih.gov/25884176/

9. Safety & Efficacy of Nicotinamide Riboside Supplementation for Improving Physiological Function in Middle-Aged and Older Adults. https://clinicaltrials.gov/ct2/show/NCT02921659

10. Braidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis. Exp Gerontol. 2020 Apr;132:110831. https://pubmed.ncbi.nlm.nih.gov/31917996/

11. Wang S, Xing Z, Vosler PS, Yin H, Li W, Zhang F, Signore AP, Stetler RA, Gao Y, Chen J. Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair. Stroke. 2008 Sep;39(9):2587-95. https://pubmed.ncbi.nlm.nih.gov/18617666/

12. Rajman, Luis et al. “Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence.” Cell metabolism vol. 27,3 (2018): 529-547. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6342515/

13. Heer C, et al, Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity. Journal of Biological Chemistry. Volume 295, Issue 52, Dec 2020. https://www.jbc.org/article/S0021-9258(17)50676-6/fulltext

14. Mehmel, Mario et al. “Nicotinamide Riboside-The Current State of Research and Therapeutic Uses.” Nutrients vol. 12,6 1616. 31 May. 2020, doi:10.3390/nu12061616 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352172/

15. Naltrexone (Oral Route). https://www.mayoclinic.org/drugs-supplements/naltrexone-oral-route/description/drg-20068408

16. Pilot Study Into LDN and NAD+. https://clinicaltrials.gov/ct2/show/NCT04604704

17. Hwang, Eun Seong, and Seon Beom Song. “Possible Adverse Effects of High-Dose Nicotinamide: Mechanisms and Safety Assessment.” Biomolecules vol. 10,5 687. 29 Apr. 2020. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7277745/

18. Cantó, Carles et al. “NAD(+) Metabolism and the Control of Energy Homeostasis: A Balancing Act between Mitochondria and the Nucleus.” Cell metabolism vol. 22,1 (2015): 31-53. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4487780/