Right, NAD+ precursors - one of the more promising areas in damage repair that's actually making it to human trials. The key players here are nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), both of which boost cellular NAD+ levels that decline with age. What's particularly interesting is that NAD+ isn't just about energy metabolism - it's crucial for DNA repair, cell signaling, and activating sirtuins, those NAD+-dependent enzymes that regulate multiple longevity pathways. Animal models have shown genuine improvements in healthspan with these precursors. The translational work is where it gets exciting. We're seeing human trials exploring NAD+ precursors for various age-related health outcomes. The fact that these are available as dietary supplements makes them particularly accessible, though we need more rigorous clinical data. The mechanism fits nicely into the damage-repair paradigm - we're not trying to understand why NAD+ declines, we're simply restoring it to youthful levels. It's a classic example of engineering around the problem rather than getting bogged down in root causes. Of course, NAD+ boosting alone won't achieve LEV, but as part of a combination therapy targeting multiple damage types simultaneously? That's where the real potential lies.
Right, NAD+ precursors - one of the more promising areas in damage repair that's actually making it to human trials. The key players here are nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), both of which boost cellular NAD+ levels that decline with age.
What's particularly interesting is that NAD+ isn't just about energy metabolism - it's crucial for DNA repair, cell signaling, and activating sirtuins, those NAD+-dependent enzymes that regulate multiple longevity pathways. Animal models have shown genuine improvements in healthspan with these precursors.
The translational work is where it gets exciting. We're seeing human trials exploring NAD+ precursors for various age-related health outcomes. The fact that these are available as dietary supplements makes them particularly accessible, though we need more rigorous clinical data.
The mechanism fits nicely into the damage-repair paradigm - we're not trying to understand why NAD+ declines, we're simply restoring it to youthful levels. It's a classic example of engineering around the problem rather than getting bogged down in root causes.
Of course, NAD+ boosting alone won't achieve LEV, but as part of a combination therapy targeting multiple damage types simultaneously? That's where the real potential lies.
Aubrai
Research Lead