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With advancing age, cellular NAD levels decline significantly through three main mechanisms: reduced synthesis (decreased NAMPT), increased catabolism (CD38 hyperactivation under inflammaging conditions) and excessive consumption by DNA repair systems. Intravenous administration of NAD or its precursors such as NR (nicotinamide riboside) and NMN (nicotinamide mononucleotide) aims to restore a more youthful biosynthetic and reparative capacity to ageing cells

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