Nicotinamide mononucleotide: Difference between revisions

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==Potential benefits and risks==
==Potential benefits and risks==


NMN is a precursor for [[Nicotinamide adenine dinucleotide|NAD<sup>+</sup>]] biosynthesis, and NMN dietary supplementation has been demonstrated to increase NAD<sup>+</sup> concentration and thus has the potential to mitigate aging-related disorders such as [[oxidative stress]], [[DNA damage (naturally occurring)|DNA damage]], [[Neurodegenerative disease|neurodegeneration]] and [[inflammation|inflammatory responses]].<ref name = Song2023>Song Q, Zhou X, Xu K, Liu S, Zhu X, Yang J. The Safety and Antiaging Effects of Nicotinamide Mononucleotide in Human Clinical Trials: an Update. Adv Nutr. 2023 Nov;14(6):1416-1435. doi: 10.1016/j.advnut.2023.08.008. Epub 2023 Aug 22. PMID: 37619764; PMCID: PMC10721522</ref> The potential benefits and risks of NMN supplementation, as of 2023, are currently under investigation.
NMN is a precursor for [[Nicotinamide adenine dinucleotide|NAD<sup>+</sup>]] biosynthesis, and NMN dietary supplementation has been demonstrated to increase NAD<sup>+</sup> concentration and thus has the potential to mitigate aging-related disorders such as [[oxidative stress]], [[DNA damage (naturally occurring)|DNA damage]], [[Neurodegenerative disease|neurodegeneration]] and [[inflammation|inflammatory responses]]. Song Q, Zhou X, Xu K, Liu S, Zhu X, Yang J. The Safety and Antiaging Effects of Nicotinamide Mononucleotide in Human Clinical Trials: an Update. Adv Nutr. 2023 Nov;14(6):1416-1435. doi: 10.1016/j.advnut.2023.08.008. Epub 2023 Aug 22. PMID: 37619764; PMCID: PMC10721522</ref> The potential benefits and risks of NMN supplementation, as of 2023, are currently under investigation.


Certain enzymes are sensitive to the intracellular NMN/[[Nicotinamide adenine dinucleotide|NAD<sup>+</sup>]] ratio, such as [[SARM1]], a protein responsible for initiating cellular degeneration pathways such as [[MAP kinase]] and inducing [[axon|axonal]] loss and [[necrosis|neuronal death]]. [[NMNAT1|NMNAT]] is an enzyme with neurorescuing properties that functions to deplete NMN and produce NAD<sup>+</sup>, attenuating SARM1 activity and aiding neuronal survival ''in-vitro'', an effect that is reversed by applying exogenous NMN which promptly resumed axon destruction. The similar molecule nicotinic acid mononucleotide (NaMN) opposes the activating effect of NMN on [[SARM1]], and is a neuroprotector.
Certain enzymes are sensitive to the intracellular NMN/[[Nicotinamide adenine dinucleotide|NAD<sup>+</sup>]] ratio, such as [[SARM1]], a protein responsible for initiating cellular degeneration pathways such as [[MAP kinase]] and inducing [[axon|axonal]] loss and [[necrosis|neuronal death]]. [[NMNAT1|NMNAT]] is an enzyme with neurorescuing properties that functions to deplete NMN and produce NAD<sup>+</sup>, attenuating SARM1 activity and aiding neuronal survival ''in-vitro'', an effect that is reversed by applying exogenous NMN which promptly resumed axon destruction. The similar molecule nicotinic acid mononucleotide (NaMN) opposes the activating effect of NMN on [[SARM1]], and is a neuroprotector.