Yamamoto T, Byun J, Zhai P, Ikeda Y, Oka S, Sadoshima J (2014) Nicotinamide Mononucleotide, an Intermediate of NAD+ Synthesis, Protects the Heart from Ischemia and Reperfusion. PLoS ONE 9(6): e98972. doi:10.1371/journal.pone.0098972 write “Nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme for nicotinamide adenine dinucleotide (NAD+) synthesis, and Sirt1, an NAD+-dependent histone deacetylase, protect the heart against ischemia/reperfusion (I/R). It remains unknown whether Nampt mediates the protective effect of ischemic preconditioning (IPC), whether nicotinamide mononucleotide (NMN, 500 mg/kg), a product of Nampt in the NAD+ salvage pathway, mimics the effect of IPC, or whether caloric restriction (CR) upregulates Nampt and protects the heart through a Sirt1-dependent mechanism. IPC upregulated Nampt protein, and the protective effect of IPC against ischemia (30 minutes) and reperfusion (24 hours) was attenuated at both early and late phases in Nampt +/− mice, suggesting that Nampt plays an essential role in mediating the protective effect of IPC. In order to mimic the effect of Nampt, NMN was administered by intraperitoneal injection. NMN significantly increased the level of NAD+ in the heart at baseline and prevented a decrease in NAD+ during ischemia.”

Disclaimer: The research paper, Nicotinamide Mononucleotide, an Intermediate of NAD+ Synthesis, Protects the Heart from Ischemia and Reperfusion, does not necessarily reference or specifically contemplate the specific NAD+ infusion therapy provided by Luna Living; but instead, discusses the benefits of NAD treatment and research more generally.

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Weill Cornell Medical College professor, Dr. Anthony A. Sauve, stated in his article, NAD+ and Vitamin B3: From Metabolism to Therapies published in The Journal of Pharmacology and Experimental Therapies, Vol. 324, No. 3 that “Chronic disease such as Parkinson’s and Alzheimer’s, are still somewhat poorly understood. Nevertheless, recent evidence is starting to suggest that chronic neurodegenerative disorders affect NAD+ metabolism adversely and may respond favorably to interventions that target NAD+ metabolism. For example, it has been known that Parkinson’s disease results in increased methylnicotinamide excretion, suggesting enhanced NAD+ breakdown. Recently, we participated in a study in which NAD metabolism was examined in transgenic mice that have a gene encoding a human amyloid precursor protein (APP). These animals develop some neuropathology of Alzheimer’s disease, such as plaque formation. Upon assay of brain tissue, NAD+ levels were decreased, and nicotinamide levels were increased in animals affected severely by disease who were on normal diets compared with animals on calorie restriction diets where the neuropathology was less severe (Qin et al., 2006). NAD+ itself was implicated in mitigating disease, and exogenous NAD+ redirected how cells process amyloid precursor protein (Qin et al., 2006). It was shown that NAD+-treated cells produced less plaque-associated forms of processed APP (Aβ) through a mechanism involving up-regulation of α-secretase, which cleaves APP competitively with β- and γ-secretases preventing Aβ formation (Qin et al., 2006). Increased sirtuin (SIRT1) catalytic activity was also implicated in mediating the enhanced protection from neuropathology in cell culture and in mouse brains (Qin et al., 2006). SIRT1is transcriptionally up-regulated in neurons by calorie restriction and is activated directly by NAD+. Although the work in the area of vitamin B3 effects in neurodegenerative disorders is still very preliminary, it invites the question of how NAD+ metabolism affects long-term neurodegenerative processes and whether enhancements/modulations to NAD+ metabolism can provide therapeutically meaningful changes in long-term outcomes in these notoriously difficult to treat diseases.

Disclaimer: The paper, NAD+ and Vitamin B3: From Metabolism to Therapies, by Anthony NAD A. Sauve, does not necessarily reference or specifically contemplate the specific NAD+ infusion therapy provided by Luna Living; but instead, discusses the benefits of NAD treatment and research more generally.

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Guest J, Grant R, Mori TA, Croft KD (2014) Changes in Oxidative Damage, Inflammation and [NAD(H)] with Age in Cerebrospinal Fluid. PLoS ONE 9(1): e85335. doi:10.1371/journal.pone.0085335 write that “As inflammation and oxidative damage rise with age a decrease in available nicotinamide adenine dinucleotide (NAD+) has been observed in multiple organs of the rat [24], including the brain (data unpublished). NAD+ is a ubiquitous molecule that is required for a number of vital cellular processes. In addition to its role in cellular energy and metabolism there are several enzymes, including poly(ADP-ribose) polymerase 1 (PARP) and silent information regulators (e.g. SIRT1), that use NAD+ as their substrate [25]–[27]. Importantly PARP activation in response to DNA damage catalyzes the successive cleavage of the ADP-ribose moiety from NAD+ resulting in the formation of ribose) subunits. Under conditions of mild-to-moderate DNA damage this process facilitates DNA repair [28]. However over-activation of PARP, due to excessive DNA damage, can result in neuronal death as a consequence of decreased ATP production due to NAD+ depletion [29]–[31]. In order to preserve cellular energy and concomitantly SIRT1 (associated with maintaining cellular longevity) and PARP activity, adequate levels of NAD+ must be sustained.”

Disclaimer: The paper, Changes in Oxidative Damage, Inflammation and [NAD(H)] with Age in Cerebrospinal Fluid, does not necessarily reference or specifically contemplate the specific NAD+ infusion therapy provided by Luna Living; but instead, discusses the benefits of NAD treatment and research more generally.

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