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Increases SIRT-1 activity as a result of enhanced NAD+ salvage, leading to beneficial epigenetic and metabolic reprogramming, including increased oxidative phosphorylation (OXPHOS) and muscle stem cell activation 1-3

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Similarly, NAD + levels appear reduced in preclinical models of age-associated diseases, including ataxia-telangiectasia (A-T), mitochondrial myopathies, and Alzheimer’s disease (AD), and disease-matched clinical samples 114,242–246