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Nicotinamide Adenine Dinucleotide (NAD): Difference between revisions
Nicotinamide Adenine Dinucleotide (NAD) (view source)
Revision as of 00:31, 20 December 2023
, 20 December 2023→NAD+, Sirtuins and Longevity-Promoting Pathway
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== NAD+, Sirtuins and Longevity-Promoting Pathway == | == NAD+, Sirtuins and Longevity-Promoting Pathway == | ||
[[File:CD38-NAD+-SIRT1 Axis.png|thumb|The CD38/NAD+/SIRT1 Axis. NAD+ levels in the body can be influenced by the supplementation of precursors nicotinamide (NAM), nicotinamide riboside (NR), and nicotinamide mononucleotide (NMN). NAD+ levels decrease with age and are further metabolized by the activation of SIRT1, PARP1, SARM1, and CD38. Restoring NAD+ levels allows for an increase in SIRT1 activity due to increased substrate availability, resulting in the inhibition of age-promoting pathways and activation of adaptive and protective transcription factors and processes. The central lineage may be described as the CD38/NAD+/SIRT1 axis, and targeting this access with nutraceutical interventions may prevent the age-related decline of NAD+ levels in the body. Black lines indicate conversion or activation. Red lines indicate inhibitors or destroyers of the indicated target.{{pmid|36678315}}]] | [[File:CD38-NAD+-SIRT1 Axis.png|thumb|The CD38/NAD+/SIRT1 Axis. NAD+ levels in the body can be influenced by the supplementation of precursors nicotinamide (NAM), nicotinamide riboside (NR), and nicotinamide mononucleotide (NMN). NAD+ levels decrease with age and are further metabolized by the activation of SIRT1, PARP1, SARM1, and CD38. Restoring NAD+ levels allows for an increase in SIRT1 activity due to increased substrate availability, resulting in the inhibition of age-promoting pathways and activation of adaptive and protective transcription factors and processes. The central lineage may be described as the CD38/NAD+/SIRT1 axis, and targeting this access with nutraceutical interventions may prevent the age-related decline of NAD+ levels in the body. Black lines indicate conversion or activation. Red lines indicate inhibitors or destroyers of the indicated target.{{pmid|36678315}}|450x450px]] | ||
Disruption of proper NAD+ levels and the loss of protective sirtuin activity have emerged as prime targets for NAD+-based interventions{{pmid|28537485}}. Administration of NAD+ precursors, such as Nicotinamide Riboside (NR) and Nicotinamide Mononucleotide (NMN), has shown potential in alleviating age-related NAD+ decline and associated pathologies, particularly in the context of age-related diseases{{pmid|28899755}}{{pmid|29883761}}{{pmid|27825999}}. Aging is associated with a decreased NAD+/NADH ratio in human plasma, mainly due to the deterioration of NAD+ stores, rather than an increase in NADH{{pmid|30124109}}. Replenishing NAD+ has been shown to rescue mitochondrial regulatory function from NAD+ induced pseudohypoxic mitochondrial stress during aging{{pmid|24360282}}. | Disruption of proper NAD+ levels and the loss of protective sirtuin activity have emerged as prime targets for NAD+-based interventions{{pmid|28537485}}. Administration of NAD+ precursors, such as Nicotinamide Riboside (NR) and Nicotinamide Mononucleotide (NMN), has shown potential in alleviating age-related NAD+ decline and associated pathologies, particularly in the context of age-related diseases{{pmid|28899755}}{{pmid|29883761}}{{pmid|27825999}}. Aging is associated with a decreased NAD+/NADH ratio in human plasma, mainly due to the deterioration of NAD+ stores, rather than an increase in NADH{{pmid|30124109}}. Replenishing NAD+ has been shown to rescue mitochondrial regulatory function from NAD+ induced pseudohypoxic mitochondrial stress during aging{{pmid|24360282}}. | ||