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Aging reduces NAD+ synthesis pathways while increasing consumption by enzymes like CD38 and PARPs, activated by inflammation and damage.[13][15] CD38, an immune-related enzyme, ramps up with age, breaking down NAD+ precursors

Studies show REV-ERB and REV-ERB nuclear receptors control circadian rhythm and metabolic genes

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Concluding Remarks The development of non-cytotoxic anti-CD38 antibodies and small molecules targeting the NADase enzymatic activity of CD38 may present as an important advancement in therapies for cancers and age-related diseases, but many important questions remain about CD38 biology and potential therapeutic uses (see outstanding questions)