Suppression of chronic inflammation and maintenance of NAD+ production and circadian function may be helpful in preserving sirtuin activity and maybe robust health as we age. Various strategies for resolving the NAD+ production and consumption mismatch have been established. Find out what NAD+ is here.
Numerous studies have examined the possible benefits of NAD+ precursor supplementation. Tryptophan, nicotinamide, nicotinic acid, nicotinamide riboside (NR), and nicotinamide mononucleotide are the primary precursors and intermediates used to manufacture NAD+ (NMN).
NAMPT’s Role to Halt NAD+ Loss.
Additionally, stimulation of the rate-limiting enzyme, NAMPT, has been investigated as a means of increasing NAD+ levels. Small molecule NAMPT activators such as SBI-797812 and P7C3 represent a ground-breaking strategy for increasing intracellular NAD+ and achieving its related beneficial benefits. The suppression of an enzyme called ACMSD can increase NAD+ biosynthesis. Inhibiting ACMSD by genetic or pharmacological means increases NAD+ production and SIRT1 activity, hence improving mitochondrial function.
Other Ways to Inhibit NAD+ Loss.
NAD+ consumption can be lowered by inhibition of CD38 and PARPs. Many CD38 inhibitors have been found, including apigenin, which occurs naturally in the environment and the tiny molecule 78c. Olaparib, marketed under the trade name Lynparza, is a PARP inhibitor used as maintenance therapy for persons with BRCA-mutated advanced ovarian cancer who have not progressed after receiving treatment. Recently, the compound DSRM-3716 was discovered to be a strong inhibitor of SARM1’s NAD+ consumption activity.
To summarize, NAD+ metabolism is quite complicated and encompasses a number of pathways and metabolites that must be considered as part of our overall knowledge of the aging process.