Study summary · research use only
NAD+ and sirtuins in aging and disease
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses nicotinamide adenine dinucleotide (NAD+) as a coenzyme and regulator of NAD+-consuming enzymes including sirtuins, poly-ADP-ribose polymerases, and CD38/157 ectoenzymes. The abstract describes how NAD+ biosynthesis, particularly via nicotinamide phosphoribosyltransferase (NAMPT), and SIRT1 function together to regulate metabolism and circadian rhythm. It states NAD+ levels decline during aging and may cause defects in nuclear and mitochondrial functions contributing to age-associated pathologies, and that restoring NAD+ with intermediates has been described to ameliorate such defects. The authors suggest combining sirtuin activation with NAD+ intermediate supplementation as a possible antiaging intervention.
Abstract
Nicotinamide adenine dinucleotide (NAD(+)) is a classical coenzyme mediating many redox reactions. NAD(+) also plays an important role in the regulation of NAD(+)-consuming enzymes, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38/157 ectoenzymes. NAD(+) biosynthesis, particularly mediated by nicotinamide phosphoribosyltransferase (NAMPT), and SIRT1 function together to regulate metabolism and circadian rhythm. NAD(+) levels decline during the aging process and may be an Achilles' heel, causing defects in nuclear and mitochondrial functions and resulting in many age-associated pathologies. Restoring NAD(+) by supplementing NAD(+) intermediates can dramatically ameliorate these age-associated functional defects, counteracting many diseases of aging, including neurodegenerative diseases. Thus, the combination of sirtuin activation and NAD(+) intermediate supplementation may be an effective antiaging intervention, providing hope to aging societies worldwide.
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