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Can NMN Really Reverse Aging?

In 2013, Times Magazine named Dr David Sinclair to their list of “Most Influential People in the World” after he and his team of researchers were able to reverse some key aspects of aging.

They found that as we age, declining levels of the key metabolite Nicotinamide Adenine Dinucleotide (NAD+) results in loss of cellular function leading to disease and aging, and that supplementation with Nicotinamide Mononucleotide (NMN), the immediate precursor used by the body to create NAD+, can replenish stores of NAD+ and reverse the aging process.

Since then, there have been dozens of studies on restoring NAD+ levels to combat various age related diseases.

Most recently Sinclair and his team demonstrated that supplying old mice with NMN in their drinking water for 2 months greatly increased the number and size of blood vessels throughout the body, such that they were indistinguishable from young mice. In fact, the old mice who received the supplement had nearly twice the endurance as those that did not, and were as fit and strong as young mice.

WHAT IS NAD+

NAD+ is a key co-enzyme that the mitochondria in every cell of our bodies depend on to fuel all basic functions. (3,4)

NAD+ play a key role in communicating between our cells nucleus and the Mitochondria that power all activity in our cells (5,6,7)

Scientists have now confirmed a direct link between falling NAD+ levels and aging in both animal and in human subjects.

Read more about NAD+  

NAD+ DECLINES WITH AGE

As we age, our bodies produce less NAD+ and the communication between the Mitochondria and cell nucleus is impaired. (5,8,10).

Over time,  decreasing NAD+ impairs the cell’s ability to make energy, which leads to aging and disease (8, 5) and perhaps even the key factor in why we age (5).

Read more about NAD+

SUPPLEMENTS TO RESTORE NAD+

NMN is not patented and is available to purchase from several different brands. Both Elysium Health and Chromadex market NR capsules.

All have shown great promise in research with mice. While we are still awaiting publication of the first studies of humans with NMN supplements, research has shown NR is effective at elevating NAD+ levels in humans.

However, it is a question if oral supplementation with NAD+ precursors will result in some of the same health benefits demonstrated in studies with mice.

Dr Sinclair’s 2013 study used IP Injections to deliver NMN directly to the bloodstream, enabling it to reach tissues throughout the body more effectively.

In the most recent study by Dr Sinclair, they put NMN in the drinking water of mice at a dosage of 400 mg per kg of bodyweight. This would equate to several grams per day in humans and be extremely expensive.

Limited bioavailability of oral supplements is a big problem. Recent research confirms that oral supplementation of NR and NMN is subject to digestion and first pass metabolism in the liver. Very little actually makes it outside the liver to reach other tissues directly.

SUBLINGUAL DELIVERY

Injections are not feasible for most people, so a more effective delivery method is needed. Introduced in late 2017, a popular option is a Pure NMN powder that users take under the tongue (Sublingually) where it is quickly absorbed directly into the bloodstream, avoiding the digestive system entirely.

Soon you will also be able to purchase a fast dissolve tablet designed for sublingual administration, providing the same benefits as the pure powder, in a more convenient form.

New research shows that NMN and NR are mostly digested to Nicotinamide when taken as oral supplements (r). Sublingual delivery of small, hydrophilic molecules such as NMN bypass the digestive system and can be quickly absorbed to the bloodstream making it far more bioavailable than capsules.

THE PROBLEM with CAPSULES – DIGESTED IN STOMACH

It has also long been suspected that most NR is digested to NAM in the Gastro-Intestinal tract intact (r).

More recently, this research published in 2018 confirms that most oral supplements of NMN and NR are digested to NAM in the GI tract or the liver.

Future pharmacological and nutraceutical efforts to boost NAD will need to take into account the minimal oral bioavailability of NR and NMN (R)

We also showed that intravenous, but not oral administration of NR or NMN delivered intact molecules to multiple tissues (R)

Unlike in cell culture where NR and NMN are readily incorporated into NAD, oral administration fails to deliver NR or NMN to tissues (R)

Interestingly, we found that neither compound was able to enter the circulation intact in substantial quantities when delivered orally (R)

The most recent studies showing tremendous health benefits with NMN were accomplished by feeding mice very large dosages of NMN in water (r). However the dosage of 300-400 mg per kg of bodyweight used in many of these studies would equate to approximately 2,000 Mg per day for a 70 kg human. A more effective delivery method is needed !

SUBLINGUAL VS CAPSULES

Sublingual (under the tongue) delivery can provide rapid absorption via the blood vessels under the tongue rather than via the digestive tract. (r,r)

The absorption of the different molecules delivered through the sublingual route can be 3 to 10 times greater than oral route and is only surpassed by direct IV injection (r).

SUBLINGUAL CAN BE MORE BIOAVAILABLE THAN INJECTION !

With intraperitoneal injection, the primary route of absorption is via the mesenteric vessels, which drain into the portal vein and pass through the liver before reaching the bloodstream.

This means, IP avoids the GI tract, but is still sent directly to the Liver, where much of it is converted to NAD+. Elevated NAD+ in the liver is good, but its far better to reach the bloodstream with intact NMN.

Sublingual delivery is not filtered by the Liver and can reach systemic circulation intact, so can actually result in greater bioavailability that direct injection! Some examples are:

  • A sublingual formulation of zol… exhibited a faster rate of absorption and higher drug exposure as compared to subcutaneous injection (r)
  • sublingually administered epin… results in more rapid absorption and a higher peak plasma concentration compared to injected epin… .(r)
  • 40mg of sublingually administered pir.. was found to be as effective as a 75 mg intramuscular injection of dicl… (r)

NMN PERFECT FOR SUBLINGUAL

Depending on the molecule, Sublingual delivery can substantially improve the speed and bioavailability. Smaller molecules that are hydrophilic such as NMN are well-suited.

a drug which has been formulated for sublingual should ideally have a molecular weight of less than 500 (r)

NMN is very hydrophilic, with a molecular weight of 324, making it a perfect fit for sublingual delivery.

SHORT WINDOW FOR MAXIMUM AVAILABILITY

The chart at right is from the 2016 Mills study with mice given 300 mg/kg of bodyweight by oral gavage.

It clearly shows NMN is found in blood plasma within minutes, peaking at around 15 minutes. After that, NMN drops rapidly in blood, and appears as increased NAD+ in the liver.

Of course this is in Mice, and humans have a slower response, but we believe it is during the short time period when NMN is available in the bloodstream and can reach tissues throughout the body that the real benefits occur.

FREQUENCY – HOW OFTEN TO TAKE

Nearly all research on mice and humans using NR and NMN is focused on measuring NAD+ and the various metabolites in the Liver as it is the primary supplier of NAD+ throughout the body (r).

If elevating NAD+ in the liver is the goal, 1-2 larger dosages per day seem to be sufficient to achieve the maximum increase in liver NAD+  (r).

However, we believe supplying NMN directly to the bloodstream is more effective at increasing NAD+  not just in the Liver, but throughout the body.

Based on the short window that exogenous NMN is available in the bloodstream before being filtered out by the Liver, we believe smaller, more frequent dosages are likely more effective than 1-2 larger dosages.

Using this philosophy, many of our customers have been reporting more perceived benefit from more frequent intake, with many taking 6-12 times per day.  We recommend taking 4-8 times per day, with at least 1 hour between dosages.

CONCLUSION – WHAT WE RECOMMEND

Dr Sinclair takes 500 Mg of NMN CAPSULES per day and prescribes the same for his father, which is in line with dosages used in current and recently completed research on humans.

There is likely an upper limit on the effective dosage of NMN and NR capsules, which seems to be between 500 and 1,000 Mg per day.

We believe that sublingual delivery allows a much greater percentage of NMN to bypass the liver and reach other tissues.  

When split between multiple smaller dosages, we believe 1,000-1,500 Mg a day can be taken before reaching the limit on maximum effectiveness.

We recommend taking 1 tablet, 4 to 8 times per day.   Ideally, 1 upon waking, 1 immediately before and after exercise, and 1 before bed, with any others spread throughout the day.

NMN was able to mitigate most age-associated physiological declines in mice Treatment of old mice with NMN reversed all of these biochemical aspects of aging

Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice (mills, 2016)

Raising NAD+ levels in old mice restores mitochondrial function to that of a young mouse

Restore the mitochondrial homeostasis and key biochemical markers of muscle health in a 22-month-old mouse to levels similar to a 6-month-old mouse

Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging (Gomes, Sinclair,2013)

DNA Repair

This study showed supplementation with NMN was able to repair the DNA in cells damaged by radiation

The cells of old mice were indistinguishable from young mice after just one week of treatment.

A conserved NAD+ binding pocket that regulates protein-protein interactions during aging (Sinclair, 2017)

WEIGHT

NMN was immediately utilized and converted to NAD+ within 15 min, resulting in significant increases in NAD+ levels over 60 min

Administering NMN, a key NAD+ intermediate, can be an effective intervention to treat the pathophysiology of diet- and age-induced T2D

Surprisingly, just one dose of NMN normalized impaired glucose tolerance

Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice (Yoshino, 2011)

NAD(+) levels were increased significantly both in muscle and liver by NMN

NMN-supplementation can induce similar reversal of the glucose intolerance

NMN intervention is likely to be increased catabolism of fats NMN-supplementation does mimic exercise

Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice (Uddin, 2016)

NMN significantly increased the level of NAD+ in the heart

NMN protected the heart from I/R injury

Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and repercussion (Yamamoto, 2014)

NMN reduces vascular oxidative stress

NMN treatment normalizes aortic stiffness in old mice

NMN represents a novel strategy for combating arterial aging

Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice (de Picciotto, 2016)

NMN can reduce myocardial inflammation NMN thus can cut off the initial inflammatory signal, leading to reduced myocardial inflammation

Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure (Zhang, 2017)

ENERGY

Remarkably, NMN administered to FXN-KO mice restores cardiac function to near-normal levels.

Restoration of cardiac function and energy metabolism upon NMN supplementation

Remarkable decrease in whole-body EE and cardiac energy wasting

Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model

VISION

Exogenous NMN prevents photoreceptor degeneration and restores vision

NMN rescues retinal dysfunction in light-induced degeneration

 

NAMPT-mediated NAD+ biosynthesis is essential for vision in mice (lin, 2016)

Completed and pending publication

Beginning 2018

  • 2018 Sinclair Metrobio study – Phase 2

The Phase 1 study by Dr Sinclair has been completed, and they are ready to go forward with the Phase 2 study, so we can conclude there were positive results, and no negative side effects, else they would have to publish those immediately.

In the University of Washington study, participants are 50 healthy women between 55 and 70 years of age with slightly high blood glucose,BMI and triglyceride levels.

Using a dose of 2 capsules of 125mg NMN per day over a period of 8 weeks, researchers are testing for:

  • change in beta-cell function
  • works to control blood sugar
  • blood vessels dilate
  • effects of NMN on blood lipids
  • effects of NMN on body fat
  • markers of cardiovascular and metabolic health

The active supplementation portion of this study has ended, but testing of metabolic parameters will continue for 2 years after supplementation has ended.  So researchers know the immediate effects and  preliminary results are expected to be announced in 2018, with  final results expected in 2020.
 

New research shows that NMN and NR are mostly digested to Nicotinamide when taken as oral supplements (r). Sublingual delivery of small, hydrophilic molecules such as NMN bypass the digestive system and can be quickly absorbed to the bloodstream making it far more bioavailable than capsules.

REFERENCES:

  1. Detection and pharmacological modulation of nicotinamide mononucleotide (NMN) in vitro and in vivo (Formentini, 2009)
  2. AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity (Cato, 2009)
  3. A possibility of nutriceuticals as an anti-aging intervention: activation of sirtuins by promoting mammalian NAD biosynthesis (Imai, 2010)
  4. NAD blocks high glucose induced mesangial hypertrophy via activation of the sirtuins-AMPK-mTOR pathway (Zhuo, 2011)
  5. Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice (Yoshino, 2011)
  6. The NAD (+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity(Canto, 2012 )
  7. NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice. (Zhang, 2016)
  8. Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging (Gomes, Sinclair,2013)
  9. Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and repercussion (Yamamoto, 2014)
  10. NAD+ and sirtuins in aging and disease (Imai, 2014)
  11. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3 (Khan, 2014)
  12. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model (Long, 2015)
  13. NAD+ metabolism and the control of energy homeostasis – a balancing act between mitochondria and the nucleus (Canto, 2015)
  14. NAD+ metabolism: Bioenergetics, signaling and manipulation for therapy (Yang, 2016)
  15. NAD+ replenishment improves lifespan and healthspan in ataxia telangiectasia models via mitophagy and DNA repair( Fang, 2016 )
  16. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans(Trammell, 2016a )
  17. Nicotinamide riboside opposes type 2 diabetes and neuropathy in mice(Trammell, 2016b )
  18. β-Nicotinamide Mononucleotide, an Anti-Aging Candidate Compound, Is Retained in the Body for Longer than Nicotinamide in Rats (Kawamura, 2016)
  19. The first human clinical study for NMN has started in Japan (Tsubota, 2016)
  20. Nicotinamide mononucleotide protects against β-amyloid oligomer-induced cognitive impairment and neuronal death (Wang, 2016)
  21. Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice (Uddin, 2016)
  22. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice (Mills, 2016)
  23. Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice (de Picciotto, 2016)
  24. Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer disease (Yao, 2017)
  25. Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model (Martin, 2017)
  26. Nicotinamide Mononucleotide, an NAD+ Precursor, Rescues Age-Associated Susceptibility to AKI in a Sirtuin 1-Dependent Manner (Guan, 2017)
  27. Nicotinamide mononucleotide attenuates brain injury after intracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway (Wei, 2017)
  28. Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure (Zhang, 2017)
  29. Modulating NAD+ metabolism, from bench to bedside (Auwerx, 2017)
  30. Aspects of Tryptophan and Nicotinamide Adenine Dinucleotide in Immunity: A New Twist in an Old Tale. (Rodriguez, 2017)
  31. Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice (Williams, 2017)
  32. NAMPT-mediated NAD biosynthesis as the internal timing mechanism: In NAD+ World, time is running in its own way (Poljsak, 2017)
  33. Effect of “Nicotinamide Mononucleotide” (NMN) on Cardiometabolic Function (NMN)
  34. The dynamic regulation of NAD metabolism in mitochondria (Stein, 2012)
  35. Novel NAD+ metabolomic technologies and their applications to Nicotinamide Riboside interventions (Trammel, 2016)
  36. Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans (Meydayni, 2016)
  37. A high-fat, ketogenic diet induces a unique metabolic state in mice. (Kennedy, 2007)
  38. Ketone body metabolism and cardiovascular disease.(Cotter, 2013)
  39. Ketone bodies as signaling metabolites(Newman, 2014)
  40. The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease(Youm, 2015)
  41. The effect of the Spanish Ketogenic Mediterranean Diet on nonalcoholic fatty liver disease: a pilot study.(Guisado, 2011)
  42. β-Hydroxybutyrate: A Signaling Metabolite in starvation response(Morales, 2016)
  43. Physiological roles of ketone bodies as substrates and signals in mammalian tissues(Robinson, 1980)
  44. Ketone bodies mimic the life span extending properties of caloric restriction (Veech, 2017)
  45. Novel ketone diet enhances physical and cognitive performance(Murray, 2016)
  46. Mitochondrial biogenesis and increased uncoupling protein 1 in brown adipose tissue of mice fed a ketone ester diet.
  47. Nutritional Ketosis Alters Fuel Preference and Thereby Endurance Performance in Athletes(Cox, 2013)
  48. Neuroendocrine Factors in the Regulation of Inflammation: Excessive Adiposity and Calorie Restriction (Fontana, 2009)
  49. Beta-adrenergic receptors are critical for weight loss but not for other metabolic adaptations to the consumption of a ketogenic diet in male mice(August, 2017)
  50. A randomized trial of a low-carbohydrate diet for obesity(Foster, 2003)
  51. β-Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation(Bae, 2016)
  52. The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. (Maalouf, 2009)
  53. AMPK activation protects cells from oxidative stress‐induced senescence via autophagic flux restoration and intracellular NAD + elevation (Han, 2016)
  54. Regulation of AMP-activated protein kinase by natural and synthetic activators (Hardie, 2015)
  55. Effects of Exhaustive Aerobic Exercise on Tryptophan-Kynurenine Metabolism in Trained Athletes (Strasser, 2016)
  56. PARP-1 inhibition increases mitochondrial metabolism through SIRT1 activation(Bai, 2011)
  57. Carbohydrate restriction regulates the adaptive response to fasting (Klein, 1992)
  58. Interventions to Slow Aging in Humans: Are We Ready? (longo, 2015)
  59. Extending healthy life span–from yeast to humans (longo, 2010)
  60. Dietary restriction with and without caloric restriction for healthy aging (Lee, 2016)
  61. A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan (Longo, 2015)
  62. Diet mimicking fasting promotes regeneration and reduces autoimmunity and multiple sclerosis symptoms (Longo, 2016
  63. Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle (Porter, 2015)
  64. Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice (Newman, 2017)
  65. The NAD(+)/sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling.  (Mouchiroud, 2013)
  66. NAMPT- mediated NAD(+) biosynthesis is essential for vision in mice  (Lin, 2016)
  67. NAD+ replenishment improves lifespan and healthspan in ataxia telangiectasia models via mitophagy and DNA repair( Fang, 2016 )
  68. Inhibiting poly ADP-ribosylation increases fatty acid oxidation and protects against fatty liver disease (Gariani, 2017 )
  69. Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle(Canto, 2010)
  70. The NAD (+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity(Canto, 2012 )
  71. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans(Trammell, 2016a )
  72. Nicotinamide riboside opposes type 2 diabetes and neuropathy in mice(Trammell, 2016b )
  73. Dietary leucine stimulates SIRT1 signaling through activation of AMPK (Hongliang, 2012)
  74. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3 (Khan, 2014)
  75. NAD blocks high glucose induced mesangial hypertrophy via activation of the sirtuins-AMPK-mTOR pathway (Zhuo, 2011)
  76. The effect of different exercise regimens on mitochondrial biogenesis and performance (Philander, 2014)
  77. Dietary proanthocyanidins boost hepatic NAD+ metabolism and SIRT1 expression and activity in a dose-dependent manner in healthy rats (Aragon’s, 2016)
  78. NAD+ Deficits in Age-Related Diseases and Cancer (Garrido, 2017)
  79. Anti-diabetic and anti-lipidemic effects of chlorogenic acid are mediated by ampk activation (Ong, 2013)
  80. Chlorogenic Acid Improves Late Diabetes through Adiponectin Receptor Signaling Pathways in db/db Mice (Chang, 2015)
  81. Adenosine Monophosphate (AMP)-Activated Protein Kinase: A New Target for Nutraceutical Compounds (Marin-Aguilar, 2017)
  82. The Effects of Ramadan Fasting on Body Composition, Blood Pressure, Glucose Metabolism, and Markers of Inflammation in NAFLD Patients: An Observational Trial (Mazidi, 2014)
  83. Comparative effects of carbohydrate versus fat restriction on metabolic profiles, biomarkers of inflammation and oxidative stress in overweight patients with Type 2 diabetic and coronary heart disease: A randomized clinical trial. (Raygan, 2016)
  84. Normal fasting plasma glucose and risk of type 2 diabetes diagnosis (Nichols, 2008)
  85. Are We All Pre-Diabetic? (Stokel,2016)
  86. Hepatic NAD+ deficiency as a therapeutic target for non-alcoholic fatty liver disease in aging (Zhou, 2016)
  87. Effect of exercise intensity on post-exercise oxygen consumption and heart rate recovery (Mann,2014)
  88. A 45-minute vigorous exercise bout increases metabolic rate for 14 hours (Knab,2011)
  89. Effects of high-intensity resistance training on untrained older men. II. Muscle fiber characteristics and nuclei-cytoplasmic relationships (Gerontol, 2000)
  90. Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice (Newman, 2017)
  91. A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice (Roberts, 2017)
  92. NK cells link obesity-induced adipose stress to inflammation (Wensveen, 2015)
  93. The “Big Bang” in obese fat: Events initiating obesity-induced adipose tissue inflammation (Wensveen, 2015)
  94. The impact of the Standard American Diet in rats: Effects on behavior, physiology and recovery from inflammatory injury(Totsch, 2017)
  95. Bioenergetic state regulates innate inflammatory responses through the transcriptional co-repressor CtBP (Shen, 2017)
  96. The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders (Stafstrom, 2012)
  97. Loss of NAD Homeostasis Leads to Progressive and Reversible Degeneration of Skeletal Muscle (Fredrick 2016)
  98. Digestion and absorption of NAD by the small intestine of the rat (Henderson, 1983)
  99. Effects of a wide range of dietary nicotinamide riboside (NR) concentrations on metabolic flexibility and white adipose tissue (WAT) of mice fed a mildly obesogenic diet(Shi, 2017)
  100. Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans (Brenner, 2004)
  101. Nampt Expression Decreases Age-Related Senescence in Rat Bone Marrow Mesenchymal Stem Cells by Targeting Sirt1 (Ma, 2017)
  102. NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR (Yoshino, 2017)

 

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