Heather Arranie 
Research studies conducted on animal test subjects suggest that NAD+ peptide may exhibit potential properties ranging from muscular function to mitigating age-related hormonal decline.
Findings imply that NAD+, an abbreviation for nicotinamide adenine dinucleotide, is the oxidized form of NADH and may be essential to both the metabolism of cells and their ability to communicate with one another.
What Exactly is NAD+ Peptide?
Investigations purport that NAD+, also known as nicotinamide adenine dinucleotide, is a molecule that may function as a signaling molecule, an electron transporter, and a coenzyme. During normal aging, the concentration of NAD+ in cells might shift. The manipulation of NAD+ levels may thus have positive effects, such as extending longevity and enhancing neurocognitive function [i].
Researchers and licensed professionals speculate that within the mitochondria lies an extremely high concentration of NAD+. It is considered necessary for the addition of poly-ADP ribose to proteins as well as the deacetylating activity of sirtuin enzymes, all of which are essential for the proliferation of cells, the metabolism of energy, the resistance to stress, the control of inflammation, and the operation of neurons [ii].
NAD+ Peptide Properties
NAD+ has been suggested to have host potential in a variety of physiological processes, particularly within the context of neurodegenerative disorders [iii].
Researchers at the Keio University School of Medicine are conducting a phase II investigation exploring the potential action of this chemical. In this study, they are investigating the possible effects of NMN (a NAD+ precursor) on glucose metabolism. Another study conducted at Hiroshima University is investigating the effect that presenting NMN supplements over an extended period may have on hormone levels [iv].
Researchers have suggested some changes in NAD+ may induce effects on the brain, and the neuroprotective properties of NAD+ have been speculated in animal-based studies. Scientists and professionals hypothesize that NAD+ peptide may help to defend against cognitive impairment and neuroinflammation, protect the mitochondria, reduce reactive oxygen species (ROS) through SIRT1 activation, and improve cognitive performance in research models exhibiting neurocognitive problems or traumatic brain damage [v, vi, vii, viii, ix].
NAD+ Peptide and Rehabilitation and Addiction Research
Recent research has suggested that NAD+ may impact the signaling mechanisms and pathways involved in the neurobiology of addiction [x].
During withdrawal recovery, disruption of the circadian rhythm, endocrine dysregulation, and variations in the dopamine system have all been linked to addiction-formed signaling. Dopamine is known to have a degenerative effect on neuronal cells; however, increasing adenosine levels with NAD+ may mitigate this effect. [xi]
NAD+ Peptide and Aging Research
Research on mice has suggested that elevating NAD+ metabolism may slow age-associated disorder progression [xii].
The continuous presentation of the NAD+ precursor NMN, tested on rodents for 12 months, appeared to have prevented the animals from gaining weight, increased their energy metabolism, and improved their sensitivity to insulin. The study’s authors hypothesized that NMN might have a prophylactic impact on the physiological changes connected with aging, and they expressed the hope that their findings could be repeated in future, more advanced research endeavors. [xiii].
Researchers speculate that constant presentation with NMN may raise concerns since its effects on neurons could be poorly understood. An increase in NMN found within the cell will activate SARM1, which is responsible for axon degeneration [xiv]. This activation of SARM1 that results from constant presentation of the NAD+ precursor NMN might be “bypassed” with NAD+ alternatives.
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References
[i] Verdin, E. (2015) “NAD + in aging, metabolism, and neurodegeneration,” Science, 350(6265), pp. 1208–1213. Available at: https://doi.org/10.1126/science.aac4854.
[ii] (no date) Nature news. Nature Publishing Group. Available at: https://www.nature.com/articles/d42473-022-00002-7
[iii] Belenky, P., Bogan, K.L. and Brenner, C. (2007) “NAD+ metabolism in health and disease,” Trends in Biochemical Sciences, 32(1), pp. 12–19. Available at: https://doi.org/10.1016/j.tibs.2006.11.006.
[iv] Kropotov, A. et al. (2021) “Equilibrative nucleoside transporters mediate the import of nicotinamide riboside and nicotinic acid riboside into human cells,” International Journal of Molecular Sciences, 22(3), p. 1391. Available at: https://doi.org/10.3390/ijms22031391.
[v] Zhao, Y. et al. (2021) “NAD+ improves cognitive function and reduces neuroinflammation by ameliorating mitochondrial damage and decreasing ROS production in chronic cerebral hypoperfusion models through SIRT1/PGC-1α Pathway,” Journal of Neuroinflammation, 18(1). Available at: https://doi.org/10.1186/s12974-021-02250-8.
[vi] Campbell, J.M. (2022) “Supplementation with NAD+ and its precursors to prevent cognitive decline across disease contexts,” Nutrients, 14(15), p. 3231. Available at: https://doi.org/10.3390/nu14153231.
[vii] Lautrup, S. et al. (2019) “NAD+ in Brain aging and neurodegenerative disorders,” Cell Metabolism, 30(4), pp. 630–655. Available at: https://doi.org/10.1016/j.cmet.2019.09.001.
[viii] Zhou, M. et al. (2015) “Neuronal death induced by misfolded prion protein is due to NAD+ depletion and can be relieved in vitro and in vivo by NAD+ replenishment,” Brain, 138(4), pp. 992–1008. Available at: https://doi.org/10.1093/brain/awv002.
[ix] A case of parkinson’s disease symptom reduction with intravenous NAD (2019). Available at: https://www.researchgate.net/publication/332440047_A_Case_of_Parkinson’s_Disease_Symptom_Reduction_with_Intravenous_NAD
[x] Braidy, N., Villalva, M.D. and Eeden, S.van (2020) “Sobriety and satiety: Is NAD+ the answer?,” Antioxidants, 9(5), p. 425. Available at: https://doi.org/10.3390/antiox9050425.
[xi] Zhang, J. et al. (2018) “Extracellular degradation into adenosine and the activities of adenosine kinase and AMPK mediate extracellular NAD+-produced increases in the adenylate pool of BV2 microglia under basal conditions,” Frontiers in Cellular Neuroscience, 12. Available at: https://doi.org/10.3389/fncel.2018.00343.
[xii] Zhang, H. et al. (2016) “NAD + repletion improves mitochondrial and stem cell function and enhances life span in mice,” Science, 352(6292), pp. 1436–1443. Available at: https://doi.org/10.1126/science.aaf2693.
[xiii] Mills, K.F. et al. (2016) “Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice,” Cell Metabolism, 24(6), pp. 795–806. Available at: https://doi.org/10.1016/j.cmet.2016.09.013.
[xiv] DiAntonio, A. (2019) “Axon degeneration: Mechanistic insights lead to therapeutic opportunities for the prevention and treatment of peripheral neuropathy,” Pain, 160(1). Available at: https://doi.org/10.1097/j.pain.0000000000001528.
