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Anti-Aging & Langlebigkeit

NAD+ (Nicotinamidadenindinukleotid)

Langlebigkeitskern

The central electron carrier of cellular metabolism and obligate substrate for sirtuins (SIRT1–7), PARPs, and CD38. Declines 50% between ages 40–60.

AminosäurenCoenzym
Mol. Gewicht663.4 Da
HalbwertszeitMinuten (direkt); Stunden (über NMN/NR)
Verfügbarkeit ✅ Auf Lager
Aminosäuresequenz Dinucleotide coenzyme

What Is NAD+?

Nicotinamide Adenine Dinucleotide (NAD+) is a coenzyme found in all living cells. It is the obligate electron carrier in oxidative phosphorylation and the essential substrate for three longevity-regulating enzyme families: sirtuins (SIRT1–7), PARPs, and CD38. NAD+ levels decline ~50% between ages 40–60 — a decline now considered a primary molecular driver of biological aging.

Schlüsselmechanismen

  • Sirtuin activation (SIRT1–7) — deacetylases that regulate mitochondrial biogenesis, DNA repair, and metabolic homeostasis
  • PARP-mediated DNA repair — repairs up to 70,000 single-strand DNA breaks per cell per day
  • Complex I electron transport — NADH donates electrons to the mitochondrial ETC — rate-limiting for ATP production
  • Circadian clock regulation — SIRT1 deacetylates core clock proteins BMAL1 and PER2
  • AMPK cross-talk — via SIRT1→LKB1→AMPK axis, drives catabolic/repair longevity states

Forschungsanwendungen

  • Mitochondrial rejuvenation and age-related muscle decline
  • DNA damage and repair kinetics in aging models
  • Metabolic health and insulin sensitivity
  • Neurodegeneration (Alzheimer's, Parkinson's preclinical models)
  • Circadian biology research

Wichtige Referenzen

  1. Gomes AP et al. “Declining NAD+ induces a pseudohypoxic state during aging.” Cell, 2013;155(7):1624–1638.
  2. Verdin E. “NAD+ in aging, metabolism, and neurodegeneration.” Science, 2015;350(6265):1208–1213.
  3. Yoshino M et al. “NMN increases muscle insulin sensitivity in prediabetic women.” Science, 2021;372:1224–1229.
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