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NADFaq.com

Benefit

Immune Function

CD38, T-cell metabolism, and immunosenescence.

Emerging human evidence

Age-related NAD+ decline is driven in large part by CD38 upregulation on macrophages and other immune cells, tying NAD+ metabolism directly to immunosenescence. T-cell activation, differentiation, and effector function depend on NAD+-fueled glycolysis and oxidative phosphorylation. Human interventional data is limited; most evidence is mechanistic or from aged-mouse models.

Key studies

  1. Cell Metabolism · 2016 · PMID 27304511

    CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism

    Camacho-Pereira J, et al.

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  2. Nature Cell Biology · 2019 · PMID 31386062

    NAD+ metabolism governs the proinflammatory senescence-associated secretome

    Nacarelli T, et al.

  3. Cell Metabolism · 2018 · PMID 29514063

    Quantitative analysis of NAD synthesis-breakdown fluxes

    Liu L, et al.

Editorial note

NADFaq grades evidence on a 4-tier scale based on human trial quality, sample size, reproducibility, and mechanistic plausibility. This is a conservative framework — many published benefits of NAD+ precursors rest on preclinical (rodent or cell) work that has not yet translated to humans.

How we grade evidence