By Stephen Harrington
Scientists are discovering new ways that NAD+ facilitates healthy longevity.1-3
NAD+ levels markedly decline with age, creating an energy deficit that decreases the body’s ability to retain youthful function.4
To give you an idea how impactful NAD+ can be, by age 50 a typical person may have only half the NAD+ they did in youth. By age 80, NAD+ levels drop to only 1% to 10% expressed in youth.
Deficiency of NAD+ predisposes us to accelerated aging and impedes our ability to fully benefit from resveratrol.
Fortunately, it is easy to restore your cellular NAD+ to higher ranges.
As a co-factor in cell energy transfer, NAD+ plays a critical role in regulating aging processes.
NAD+ is the acronym for nicotinamide adenine dinucleotide.
Found in virtually all living cells, NAD+ is essential to sustaining life.4
A fascinating aspect of NAD+ is its dual role in protecting against factors that age us. This includes mitigating chemical stress, inflammation, DNA damage, and failing mitochondria.
At the same time, NAD+ promotes longevity by facilitating DNA repair and providing cellular benefits associated with caloric restriction and exercise.5
In other words, while a decline in NAD+ levels may negatively influence lifespan, restoring NAD+ is increasingly being viewed as a cutting-edge tool to promote longevity.
There is growing evidence that supplementing with a vitamin-like precursor of NAD+ called nicotinamide riboside can promote longevity in life forms ranging from simple worms to mammals like mice.5-11
One study showed an average 5% increase in the lifespan of old mice—even though supplementation did not begin until the mice were nearing the end of their natural lifespan (24 months).11
That would be the equivalent of gaining nearly an additional four years of life based on today’s average human expectancy of 78.8 years.12
A rigorous scientific review of NAD+ reveals that its longevity benefits arise from eight different, but interrelated, functions.
This article briefly summarizes each anti-aging mechanism played by NAD+ in your body.
Anti-Aging Mechanism #1:
NAD+ May Contribute to Longer Telomeres
NAD+ is required for functioning of the sirtuin proteins that contribute to longevity—and specifically to maintaining the length of critical telomeres.
Telomeres are stretches of repetitive DNA strands that cap the ends of chromosomes. Like the burning of a fuse, telomeres at the ends of our chromosomes steadily shorten every time a cell replicates itself. Once telomeres reach a critically short length, cell renewal virtually stops, leading to accelerated aging or death of the cell.13
Telomere shortening is both a marker of cellular aging and a predictor of shortened lifespan.14
Researchers have been searching for drugs and other interventions that might lengthen telomeres, in order to extend lifespan and/or health span. To date, exercise and weight loss have been reliably shown to be effective at telomere lengthening.15-17
Certain other nutrients, such as resveratrol, may activate sirtuins and contribute to extending lifespan, but emerging evidence suggests sirtuins function best with an ample supply of NAD+.
Conclusion: The possibility of extending telomere length with NAD+ holds out hope for slowing the aging process and improving longevity.
WHAT YOU NEED TO KNOW
Restore Cellular Energy with NAD+
- NAD+ is required for proper cellular energy utilization, but its levels decline with age.
- It is also required for eight fundamental processes, each of which contributes to accelerated aging when NAD+ levels drop.
- NAD+ is unstable and cannot be used as a supplement, but nicotinamide riboside is a useful precursor to NAD+ that is capable of restoring cellular NAD+ levels.
- Studies show that nicotinamide riboside supplementation can slow cellular aging and improve many of the metabolic defects common to the aging process, including obesity, diabetes, cardiovascular disease, and neurodegenerative conditions.
- Supplementation with nicotinamide riboside offers a way of supporting essential body systems.
Anti-Aging Mechanism #2:
NAD+ Promotes DNA Repair
Even though DNA is protected by its chromosomal shelter, it is highly vulnerable to damage.
This can lead to broken DNA strands and mutations in crucial genes. Accumulated DNA damage contributes to the aging process and can result in specific lifespan-shortening diseases like cancer and poor immune function.18
When DNA is damaged, it activates an enzyme known as PARP-1 that carries out DNA repair within cells.19To carry out its function, PARP-1 consumes enormous amounts of NAD+. As NAD+ is depleted, the ability of PARP-1 to repair DNA is significantly hindered.19-28
The good news is that replenishing NAD+ to cells can restore DNA repair and prevent cell death under stress.26,29 In two different animal models of neurodegenerative disease, increasing cellular NAD+ reduced the severity of the disorder, normalized neuromuscular function, delayed memory loss, and extended lifespan.30
Conclusion: Improving DNA repair with NAD+ may slow cellular aging, reduce the persistence of cancer-causing mutations, and play an important role in preventing inflammatory conditions such as atherosclerosis.31,32
Normal aging may one day be classified as “NAD+ deficiency syndrome.”
Fortunately, there are proven ways to boost NAD+ levels.
Anti-Aging Mechanism #3:
NAD+ Modulates Immune-Cell Signaling
As we age, our immune cells begin to lose their focus. Some become overactive, contributing to autoimmune disease, while others slow down, which increases the risk of infection. This process, called immunosenescence, is intimately related to mitochondrial function and energy balance,33 both of which depend on NAD+ activity.
Intracellular levels of NAD+ regulate immune and inflammatory pathways, including the cytokine TNF-alpha, a critical signaling molecule.34,35
Conclusion: Adequate intracellular NAD+ is vital for youthful cellular energy, a critically important factor in fending off immunosenescence and maintaining defenses against infections and autoimmune disease.
Anti-Aging Mechanism #4:
NAD+ Induces Energy-Intensive Enzymes
A universal feature of aging is the loss of cellular energy, which results in diminished ATP levels and inadequate cellular fuel necessary to power your body.23,36,37
One cause of this energy loss is a breakdown in the efficiency of the electron transport chain, the main pathway through which we extract energy from food (and of which NAD+ is an essential component).23,38Disorders ranging from obesity and diabetes to bone loss have been associated with loss of this vital pathway.38,39
Studies now show that restoring electron transport chain function by raising levels of NAD+ is a rapid and efficient means of promoting the essential enzymes involved in energy extraction and sustaining youthful cell function. This helps to reduce physiological decline and provides protection from age-related disease.22,40
Conclusion: Improving the energy-extraction process in all cells with NAD+ increases their capacity to do the work they are specialized for. It also protects mitochondria from early death, a benefit that is associated with reduced cellular aging and lowered risks for cardiovascular and brain disease.41-45
Anti-Aging Mechanism #5:
NAD+ Promotes Chromosome Stability
Our chromosomes are complex structures housing our DNA. Access to DNA strands for “reading out” genetic instructions requires biochemical control of those proteins to make sure each gene functions properly.46
But like any complex molecular structure, chromosomes can become unstable. Eventually, this triggers errors in the ways our genes are interpreted—which ultimately contributes to deleterious changes in cell function and structure. Aging is accelerated in the presence of increased chromosome instability.47-49
The enzymes involved in sustaining stable chromosomal structures require NAD+ in order to function properly.
In animal models showing that NAD+ contributes to longevity, a major factor has been shown to be sufficient availability of the nutrient.46,50,51 And studies show that when enzymes that require NAD+ are inactive, chromosome structure suffers and cells replicate abnormally.50
Conclusion: NAD+ supplementation is a promising cutting edge strategy to improve chromosome stability, a treatment that may slow down cellular aging (senescence) and lower the risk of cancer.
Anti-Aging Mechanism #6:
NAD+ Is a Neurotransmitter
Neurotransmitters are brain chemicals that relay signals between nerve cells. In doing so, they help regulate body-wide functions such as mood, appetite, and stress.
NAD+ has been found to meet all criteria for a neurotransmitter.52,53
Evidence for NAD+’s neurotransmitter function has now been found in intestinal and blood vessel smooth muscles, as well as in the brain itself.52
Conclusion: Ample NAD+ nutrition appears essential for sustaining brain health.
Anti-Aging Mechanism #7:
NAD+ Activates Sirtuins
Proteins called sirtuins are major regulators of cellular aging because they influence fundamental functions such as DNA repair and inflammatory responses. They also influence whether cells enter a replicative cycle or instead die a programmed death (apoptosis).53
Compounds that activate sirtuins are eagerly sought as chemical “fountains of youth.” Familiar supplements like resveratrol and quercetin have been evaluated as promising sirtuin activators.2,54-56
NAD+ is required for sirtuins to function.57-59
Conclusion: Sirtuin activation has shown great promise in fighting cardiovascular disease and preserving aging brain function, but these longevity-promoters cannot function without sufficient NAD+.4,54
Anti-Aging Mechanism #8:
NAD+ Supports Energy Production
NAD+ was first discovered as an important part of the process that channels chemical energy from foods to the ATP fuel our cells require. Recent studies have revealed that NAD+ is itself a form of “energy currency” similar to ATP.60
NAD+ is also a functional signaling molecule in processes related to energy production, including PARP-1 and sirtuins. When DNA damage occurs, PARP-1 consumes large quantities of NAD+, leading to reduced energy production. In addition, high levels of NAD+ can activate sirtuins, permitting them to carry out their metabolic and stress-protective responses and contributing to longevity.23
Conclusion: Supporting efficient energy production and adequate ATP levels requires consistent and abundant NAD+. This is critical because waning energy supplies contribute to the aging process.
How to Boost NAD+
NAD+ is biologically unstable, which makes it unsuitable for oral supplementation. Fortunately, there’s a solution.
About a decade ago, researchers discovered that the compound nicotinamide riboside is rapidly converted by natural cellular enzymes into active NAD+.
Studies show that supplementing with nicotinamide riboside is an effective means of raising cellular NAD+levels.6,22,61
Nicotinamide riboside is readily available for oral supplementation, and it is highly bioavailable.62 These benefits make nicotinamide riboside the leading oral candidate to boost cellular NAD+, and research is revealing just how effective it is.63
The Metabolic Benefits of Boosting NAD+
Nicotinamide riboside boosts NAD+ and appears useful in preventing diseases associated with abnormal energy utilization. These include obesity, diabetes, and atherosclerosis, which are components of metabolic syndrome.
A mouse study revealed that prediabetic mice given nicotinamide riboside have better glucose tolerance, less weight gain and liver damage, and slower development of fatty livers. Similarly, in diabetic mice, nicotinamide riboside markedly reduced blood sugar, weight gain, and liver fat, while also preventing diabetic nerve damage.64
Nicotinamide riboside is especially beneficial in combatting nonalcoholic fatty liver disease (NAFLD), which is considered the liver manifestation of metabolic syndrome. Interventions that reduce NAFLD generally improve all-around metabolic health.
Studies in animal models of NAFLD have shown that nicotinamide riboside supplementation corrects biochemical and microscopic liver changes in mice fed a high-fat diet.65,66
In another study of obesity induced by a high-fat diet, supplementation with nicotinamide riboside increased NAD+ levels, activated sirtuins, and protected against the oxidative stresses and other damage induced by the diet (many of NAD+’s longevity mechanisms mentioned above).22
Additional NAD+ Benefits
Brain tissue is highly sensitive to alterations in NAD+ levels.67 A mouse study showed that supplementation with nicotinamide riboside increased NAD+ levels in the brain, slowed cognitive decline in mice with Alzheimer’s, and enhanced the plasticity in neurons that underlies learning and memory.67
Regular exercise is a panacea for most of the age-accelerating processes in our bodies. Recent studies are showing that nicotinamide riboside helps improve exercise performance by improving mitochondrialdynamics and muscle function.68
And in animals that had undergone removal of part of their livers, researchers showed that nicotinamide riboside supplementation promoted new DNA synthesis, cell replication, and increased liver mass—a vivid demonstration of its healing powers.69
NAD+ beneficially enhances eight core cellular anti-aging mechanisms.
When these cell functions are impaired, the consequence is accelerated aging that contributes to disorders as diverse as Alzheimer’s and osteoporosis.
Restoring cell NAD+ levels has been shown to preserve youthful function—and even reverse some age-induced deterioration.
Nicotinamide riboside has been shown not only to restore NAD+ levels in tissues, but also to provide more NAD+ activity than can be obtained from diet alone.
Supplementation with nicotinamide riboside can slow cellular aging and improve many metabolic defects common to degenerative processes, including diabetes, declining heart function and neurodegenerative conditions.
If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.
- Imai S. The NAD World: a new systemic regulatory network for metabolism and aging–Sirt1, systemic NAD biosynthesis, and their importance. Cell Biochem Biophys. 2009;53(2):65-74.
- Bonkowski MS, Sinclair DA. Slowing ageing by design: the rise of NAD+ and sirtuin-activating compounds. Nat Rev Mol Cell Biol. 2016;17(11):679-90.
- Imai SI. The NAD World 2.0: the importance of the inter-tissue communication mediated by NAMPT/NAD+/SIRT1 in mammalian aging and longevity control. NPJ Syst Biol Appl. 2016;2:16018.
- Imai SI, Guarente L. It takes two to tango: NAD+ and sirtuins in aging/longevity control. NPJ Aging Mech Dis.2016;2:16017.
- Poljsak B, Milisav I. NAD+ as the Link Between Oxidative Stress, Inflammation, Caloric Restriction, Exercise, DNA Repair, Longevity, and Health Span. Rejuvenation Res. 2016.
- Belenky P, Racette FG, Bogan KL, et al. Nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+. Cell. 2007;129(3):473-84.
- Denu JM. Vitamins and aging: pathways to NAD+ synthesis. Cell. 2007;129(3):453-4.
- Lu SP, Kato M, Lin SJ. Assimilation of endogenous nicotinamide riboside is essential for calorie restriction-mediated life span extension in Saccharomyces cerevisiae. J Biol Chem. 2009;284(25):17110-9.
- Mouchiroud L, Houtkooper RH, Moullan N, et al. The NAD(+)/Sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling. Cell. 2013;154(2):430-41.
- Tsang F, James C, Kato M, et al. Reduced Ssy1-Ptr3-Ssy5 (SPS) signaling extends replicative life span by enhancing NAD+ homeostasis in Saccharomyces cerevisiae. J Biol Chem. 2015;290(20):12753-64.
- Zhang H, Ryu D, Wu Y, et al. NAD(+) repletion improves mitochondrial and stem cell function and enhances life span in mice. Science. 2016;352(6292):1436-43.
- Available at: https://www.cdc.gov/nchs/fastats/life-expectancy.htm. Accessed November 15, 2017.
- Gopalakrishnan S, Cheung NK, Yip BW, et al. Medaka fish exhibits longevity gender gap, a natural drop in estrogen and telomere shortening during aging: a unique model for studying sex-dependent longevity. Front Zool. 2013;10(1):78.
- Heidinger BJ, Blount JD, Boner W, et al. Telomere length in early life predicts lifespan. Proc Natl Acad Sci U S A. 2012;109(5):1743-8.
- Carulli L, Anzivino C, Baldelli E, et al. Telomere length elongation after weight loss intervention in obese adults. Mol Genet Metab. 2016;118(2):138-42.
- Honka MJ, Bucci M, Andersson J, et al. Resistance training enhances insulin suppression of endogenous glucose production in elderly women. J Appl Physiol (1985). 2016;120(6):633-9.
- Sjogren P, Fisher R, Kallings L, et al. Stand up for health–avoiding sedentary behaviour might lengthen your telomeres: secondary outcomes from a physical activity RCT in older people. Br J Sports Med.2014;48(19):1407-9.
- Jackson SP, Bartek J. The DNA-damage response in human biology and disease. Nature.2009;461(7267):1071-8.
- Ying W, Garnier P, Swanson RA. NAD+ repletion prevents PARP-1-induced glycolytic blockade and cell death in cultured mouse astrocytes. Biochem Biophys Res Commun. 2003;308(4):809-13.
- Dawicki-McKenna JM, Langelier MF, DeNizio JE, et al. PARP-1 Activation Requires Local Unfolding of an Autoinhibitory Domain. Mol Cell. 2015;60(5):755-68.
- Liu M, Li Z, Chen GW, et al. AG-690/11026014, a novel PARP-1 inhibitor, protects cardiomyocytes from AngII-induced hypertrophy. Mol Cell Endocrinol. 2014;392(1-2):14-22.
- Canto C, Houtkooper RH, Pirinen E, et al. The NAD(+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity. Cell Metab. 2012;15(6):838-47.
- Oka S, Hsu CP, Sadoshima J. Regulation of cell survival and death by pyridine nucleotides. Circ Res.2012;111(5):611-27.
- Bai P, Canto C, Oudart H, et al. PARP-1 inhibition increases mitochondrial metabolism through SIRT1 activation. Cell Metab. 2011;13(4):461-8.
- Strosznajder RP, Czubowicz K, Jesko H, et al. Poly(ADP-ribose) metabolism in brain and its role in ischemia pathology. Mol Neurobiol. 2010;41(2-3):187-96.
- Wang S, Xing Z, Vosler PS, et al. Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair. Stroke. 2008;39(9):2587-95.
- Diefenbach J, Burkle A. Introduction to poly(ADP-ribose) metabolism. Cell Mol Life Sci. 2005;62(7-8):721-30.
- Burkle A, Beneke S, Muiras ML. Poly(ADP-ribosyl)ation and aging. Exp Gerontol. 2004;39(11-12):1599-601.
- Pittelli M, Felici R, Pitozzi V, et al. Pharmacological effects of exogenous NAD on mitochondrial bioenergetics, DNA repair, and apoptosis. Mol Pharmacol. 2011;80(6):1136-46.
- Fang EF, Kassahun H, Croteau DL, et al. NAD+ Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair. Cell Metab. 2016;24(4):566-81.
- Borghini A, Cervelli T, Galli A, et al. DNA modifications in atherosclerosis: from the past to the future. Atherosclerosis. 2013;230(2):202-9.
- Shah NR, Mahmoudi M. The role of DNA damage and repair in atherosclerosis: A review. J Mol Cell Cardiol.2015;86:147-57.
- Rottenberg H, Wu S. Mitochondrial dysfunction in lymphocytes from old mice: enhanced activation of the permeability transition. Biochem Biophys Res Commun. 1997;240(1):68-74.
- Van Gool F, Galli M, Gueydan C, et al. Intracellular NAD levels regulate tumor necrosis factor protein synthesis in a sirtuin-dependent manner. Nat Med. 2009;15(2):206-10.
- Montecucco F, Cea M, Cagnetta A, et al. Nicotinamide phosphoribosyltransferase as a target in inflammation- related disorders. Curr Top Med Chem. 2013;13(23):2930-8.
- Medkour Y, Dakik P, McAuley M, et al. Mechanisms Underlying the Essential Role of Mitochondrial Membrane Lipids in Yeast Chronological Aging. Oxid Med Cell Longev. 2017;2017:2916985.
- Lopez-Otin C, Blasco MA, Partridge L, et al. The hallmarks of aging. Cell. 2013;153(6):1194-217.
- Ritov VB, Menshikova EV, Azuma K, et al. Deficiency of electron transport chain in human skeletal muscle mitochondria in type 2 diabetes mellitus and obesity. Am J Physiol Endocrinol Metab. 2010;298(1):E49-58.
- Shum LC, White NS, Nadtochiy SM, et al. Cyclophilin D Knock-Out Mice Show Enhanced Resistance to Osteoporosis and to Metabolic Changes Observed in Aging Bone. PLoS One. 2016;11(5):e0155709.
- Mills KF, Yoshida S, Stein LR, et al. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016;24(6):795-806.
- Marzetti E, Csiszar A, Dutta D, et al. Role of mitochondrial dysfunction and altered autophagy in cardiovascular aging and disease: from mechanisms to therapeutics. Am J Physiol Heart Circ Physiol.2013;305(4):H459-76.
- Paradies G, Paradies V, Ruggiero FM, et al. Protective role of melatonin in mitochondrial dysfunction and related disorders. Arch Toxicol. 2015;89(6):923-39.
- Udhayabanu T, Manole A, Rajeshwari M, et al. Riboflavin Responsive Mitochondrial Dysfunction in Neurodegenerative Diseases. J Clin Med. 2017;6(5).
- Yue L, Yao H. Mitochondrial dysfunction in inflammatory responses and cellular senescence: pathogenesis and pharmacological targets for chronic lung diseases. Br J Pharmacol. 2016;173(15):2305-18.
- Ziegler DV, Wiley CD, Velarde MC. Mitochondrial effectors of cellular senescence: beyond the free radical theory of aging. Aging Cell. 2015;14(1):1-7.
- Newman BL, Lundblad JR, Chen Y, et al. A Drosophila homologue of Sir2 modifies position-effect variegation but does not affect life span. Genetics. 2002;162(4):1675-85.
- Chen M, Huang JD, Deng HK, et al. Overexpression of eIF-5A2 in mice causes accelerated organismal aging by increasing chromosome instability. BMC Cancer. 2011;11:199.
- Lushnikova T, Bouska A, Odvody J, et al. Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression. Oncogene. 2011;30(46):4622-31.
- Rao CV, Asch AS, Yamada HY. Emerging links among Chromosome Instability (CIN), cancer, and aging. Mol Carcinog. 2017;56(3):791-803.
- Fatoba ST, Okorokov AL. Human SIRT1 associates with mitotic chromatin and contributes to chromosomal condensation. Cell Cycle. 2011;10(14):2317-22.
- Starai VJ, Takahashi H, Boeke JD, et al. A link between transcription and intermediary metabolism: a role for Sir2 in the control of acetyl-coenzyme A synthetase. Curr Opin Microbiol. 2004;7(2):115-9.
- Mutafova-Yambolieva VN. Neuronal and extraneuronal release of ATP and NAD(+) in smooth muscle. IUBMB Life. 2012;64(10):817-24.
- Watroba M, Dudek I, Skoda M, et al. Sirtuins, epigenetics and longevity. Ageing Res Rev. 2017;40:11-9.
- Rowlands BD, Lau CL, Ryall JG, et al. Silent information regulator 1 modulator resveratrol increases brain lactate production and inhibits mitochondrial metabolism, whereas SRT1720 increases oxidative metabolism. J Neurosci Res. 2015;93(7):1147-56.
- Hung CH, Chan SH, Chu PM, et al. Quercetin is a potent anti-atherosclerotic compound by activation of SIRT1 signaling under oxLDL stimulation. Mol Nutr Food Res. 2015;59(10):1905-17.
- Xiao N, Mei F, Sun Y, et al. Quercetin, luteolin, and epigallocatechin gallate promote glucose disposal in adipocytes with regulation of AMP-activated kinase and/or sirtuin 1 activity. Planta Med. 2014;80(12):993-1000.
- Canto C, Auwerx J. Targeting sirtuin 1 to improve metabolism: all you need is NAD(+)? Pharmacol Rev.2012;64(1):166-87.
- Landry J, Sutton A, Tafrov ST, et al. The silencing protein SIR2 and its homologs are NAD-dependent protein deacetylases. Proc Natl Acad Sci U S A. 2000;97(11):5807-11.
- Villalba JM, Alcain FJ. Sirtuin activators and inhibitors. Biofactors. 2012;38(5):349-59.
- Available at: https://www.nature.com/scitable/topicpage/cell-energy-and-cell-functions-14024533. Accessed November 15, 2017.
- Belenky P, Christensen KC, Gazzaniga F, et al. Nicotinamide riboside and nicotinic acid riboside salvage in fungi and mammals. Quantitative basis for Urh1 and purine nucleoside phosphorylase function in NAD+metabolism. J Biol Chem. 2009;284(1):158-64.
- Trammell SA, Schmidt MS, Weidemann BJ, et al. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun. 2016;7:12948.
- Chi Y, Sauve AA. Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection. Curr Opin Clin Nutr Metab Care. 2013;16(6):657-61.
- Trammell SA, Weidemann BJ, Chadda A, et al. Nicotinamide Riboside Opposes Type 2 Diabetes and Neuropathy in Mice. Sci Rep. 2016;6:26933.
- Zhou CC, Yang X, Hua X, et al. Hepatic NAD(+) deficiency as a therapeutic target for non-alcoholic fatty liver disease in ageing. Br J Pharmacol. 2016;173(15):2352-68.
- Zhang K, Kim H, Fu Z, et al. Deficiency of the Mitochondrial NAD Kinase Causes Stress-induced hepatic steatosis in mice. Gastroenterology. 2017.
- Gong B, Pan Y, Vempati P, et al. Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-gamma coactivator 1alpha regulated beta-secretase 1 degradation and mitochondrial gene expression in Alzheimer’s mouse models. Neurobiol Aging. 2013;34(6):1581-8.
- Close GL, Hamilton DL, Philp A, et al. New strategies in sport nutrition to increase exercise performance. Free Radic Biol Med. 2016;98:144-58.
- Mukherjee S, Chellappa K, Moffitt A, et al. Nicotinamide adenine dinucleotide biosynthesis promotes liver regeneration. Hepatology. 2017;65(2):616-30.