Study summary · research use only
Role of NAD(+) in regulating cellular and metabolic signaling pathways
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses NAD+ (nicotinamide adenine dinucleotide), a coenzyme present in every living cell, and its involvement in metabolic processes tied to cellular bioenergetics, often studied in the context of aging, cancer, and neurodegenerative and metabolic disorders. The authors describe cellular NAD+ depletion as associated with compromised adaptive cellular stress responses, impaired neuronal plasticity, impaired DNA repair, and cellular senescence, and summarize evidence on boosting NAD+ levels using NAD+ precursors across various diseases. The review discusses how alterations in the NAD+/NADH ratio or NAD+ pool size may contribute to neurodegenerative disorders, aging, and tumorigenesis, and notes that the direct role of impaired NAD+-dependent processes in humans remains unestablished, calling for further longitudinal research on NAD+ synthesis and degradation.
Abstract
Nicotinamide adenine dinucleotide (NAD+), a critical coenzyme present in every living cell, is involved in a myriad of metabolic processes associated with cellular bioenergetics. For this reason, NAD+ is often studied in the context of aging, cancer, and neurodegenerative and metabolic disorders. Cellular NAD+ depletion is associated with compromised adaptive cellular stress responses, impaired neuronal plasticity, impaired DNA repair, and cellular senescence. Increasing evidence has shown the efficacy of boosting NAD+ levels using NAD+ precursors in various diseases. This review provides a comprehensive understanding into the role of NAD+ in aging and other pathologies and discusses potential therapeutic targets. An alteration in the NAD+/NADH ratio or the NAD+ pool size can lead to derailment of the biological system and contribute to various neurodegenerative disorders, aging, and tumorigenesis. Due to the varied distribution of NAD+/NADH in different locations within cells, the direct role of impaired NAD+-dependent processes in humans remains unestablished. In this regard, longitudinal studies are needed to quantify NAD+ and its related metabolites. Future research should focus on measuring the fluxes through pathways associated with NAD+ synthesis and degradation.
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