NAD+

TREATMENT PROTOCOL:

Studies:

1. Therapeutic potential of boosting NAD+ in aging and age-related diseases: Emerging evidence implicates that elevation of NAD+ levels may slow or even reverse the aspects of aging and also delay the progression of age-related diseases.
2. Role of Nicotinamide Adenine Dinucleotide and Related Precursors as Therapeutic Targets for Age-Related Degenerative Diseases: Rationale, Biochemistry, Pharmacokinetics, and Outcomes:  Recent studies have shown that enhancing NAD+ levels can profoundly reduce oxidative cell damage in catabolic tissue, including the brain. Therefore, promotion of intracellular NAD+ anabolism represents a promising therapeutic strategy for age-associated degenerative diseases in general, and is essential to the effective realization of multiple benefits of healthy sirtuin activity.
3. NAD + biosynthesis, aging, and disease:  Indeed, new studies have demonstrated the therapeutic potential of supplementing NAD + intermediates, such as nicotinamide mononucleotide and nicotinamide riboside, providing a proof of concept for the development of an effective anti-aging intervention.
4. Emerging potential benefits of modulating NAD+ metabolism in cardiovascular disease:  NAD+-related metabolites have promising therapeutic effects in cardiovascular disease.
5. Therapeutic potential of NAD-boosting molecules: the in vivo evidence: Nicotinamide adenine nucleotide (NAD+) has emerged as a key regulator of cellular processes that control the body’s response to stress. Rajman et al. discuss NAD boosters, small molecules that raise NAD+ levels, which are now considered to be highly promising for the treatment of multiple diseases and the potential extension of human lifespan.
6. The NAD Deficiency Diseases: Argues that oral nicotine acid therapy provides an effective biological treatment for addiction to both alcohol and opiate drugs when given in daily doses of 500 mg or more. It is also purported that there is considerable evidence that this same treatment is effective for other manifestations of the nicotinamide adenine dinucleotide (NAD) deficiency disease like anorexia nervosa, early diabetes mellitus, heart failure, essential hypertension, schizophrenia (substrate pellagra), and even the problems of predatory behavior such as crime and violence. The author hypothesizes that NAD and the endorphins are the only 2 physiological substances that bind the so-called opiate receptors in the brain, and since the development of agriculture, humans have been susceptible to what he calls the NAD deficiency diseases, through a partial adaptation to less meat in the diet. (PsycINFO Database Record (c) 2019 APA, all rights reserved)
7. Treatment with NAD(+) inhibited experimental autoimmune encephalomyelitis by activating AMPK/SIRT1 signaling pathway and modulating Th1/Th17 immune responses in mice. Nicotinamide adenine dinucleotide (NAD(+)) plays vital roles in mitochondrial functions, cellular energy metabolism and calcium homeostasis. In this study, we investigated the effect of NAD(+) administration for the treatment of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. EAE, a classical animal model of multiple sclerosis (MS), was induced by subcutaneous injection of myelin oligodendrocyteglycoprotein (MOG). The mice were treated with 250mg/kg (body weight) NAD(+) in PBS administered intraperitoneally once daily. We observed that NAD(+) treatment could lessen the severity of EAE. Additionally, NAD(+) treatment attenuated pathological injuries of EAE mice. We also found that the AMP-activated protein kinase (AMPK)/silent mating-type information regulation 2 homolog 1(SIRT1) pathway was activated in the NAD(+)-treated mice and NAD(+) treatment suppressed pro-inflammatory T cell responses. Our findings demonstrated that NAD(+) could be an effective and promising agent to treat multiple sclerosis and its effects on other autoimmune diseases should be explored.