Study summary · research use only
NAD(+) homeostasis in health and disease
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review article discusses nicotinamide adenine dinucleotide (NAD+) biology across health and disease, without describing a specific study organism (species not specified). The article traces NAD+'s conceptual shift from a simple metabolic cofactor to a cosubstrate for proteins including the sirtuin family, and it discusses reported declines in NAD+ levels during aging and altered NAD+ homeostasis in age-related conditions such as neurodegeneration, diabetes, and cancer. The authors describe various strategies for increasing NAD+ levels that have shown effects in preclinical settings, and they review the biochemistry and metabolism of NAD+ along with current challenges and translational potential for NAD+ research.
Abstract
The conceptual evolution of nicotinamide adenine dinucleotide (NAD+) from being seen as a simple metabolic cofactor to a pivotal cosubstrate for proteins regulating metabolism and longevity, including the sirtuin family of protein deacylases, has led to a new wave of scientific interest in NAD+. NAD+ levels decline during ageing, and alterations in NAD+ homeostasis can be found in virtually all age-related diseases, including neurodegeneration, diabetes and cancer. In preclinical settings, various strategies to increase NAD+ levels have shown beneficial effects, thus starting a competitive race to discover marketable NAD+ boosters to improve healthspan and lifespan. Here, we review the basics of NAD+ biochemistry and metabolism, and its roles in health and disease, and we discuss current challenges and the future translational potential of NAD+ research.
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