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Production of NAD+ declines sharply with age, leading to hidden cellular damage and visible symptoms like wrinkles, stubborn fat, cognitive fog, delayed recovery, and joint discomfort.[1][2][3] Emerging research suggests that this decline not only accelerates visible aging but also contributes to a cascade of metabolic and neurological issues, making NAD+ restoration a cornerstone of modern anti-aging protocols

Recent studies further connect sustained Ca 2+ entry (via NMDAR or P2X7) to loss of mitochondrial membrane potential, increased mitochondrial ROS, and suppression of mitophagic clearance, collectively potentiating NLRP3 activation in microglia under HIV-related conditions [100]

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