Nicotinamide adenine dinucleotide (NAD⁺) is a central redox cofactor and the limiting substrate of key metabolic enzymes that include the sirtuin family of protein deacylases, the poly(ADP-ribose) polymerases (PARPs) and the cyclic ADP-ribose (cADPr) synthases.
The constellation of cellular functions in which these enzymes are involved makes NAD⁺ availability critical for cell survival, and its depletion is a leading factor in a number of diseases in humans. Primary deficiencies of NAD⁺ homeostasis are the result of impaired biosynthesis, while secondary deficiencies can arise due to other factors affecting NAD⁺ homeostasis, such as increased NAD⁺ consumption or dietary deficiency of its vitamin B3 precursors. NAD⁺ depletion can manifest in a wide variety of pathological phenotypes, ranging from rare inherited defects to more common multifactorial, often age-related, diseases (see figure below)). In fact, exhaustion of NAD⁺ intracellular levels is currently considered a major contributor to aging, and has been associated with the onset of age-related complications such as diabetes, neurodegenerative diseases and female infertility. In contrast, NAD⁺ repletion strategies, such as administration of NAD⁺ precursors, may be effective in preventing or ameliorating the outcomes of these complications.
NAD⁺ Videos
Want to learn more about NAD⁺ research? Watch the videos below!
Metabolic networks and NAD⁺
A talk on metabolic networks and NAD⁺, given by Prof. Dr. Riekelt Houtkooper leading the consortium.
Breakthroughs in aging research
Ready to explore the latest breakthroughs in aging research? Click the link below to watch Morten Scheibye Knudsen’s lecture at ARDD 2023.
