The science of aging well. Research on NAD+ supplementation, cellular repair, telomere health, mitochondrial function, and anti-aging protocols designed to extend healthspan and optimize long-term vitality.
SARM1 is the executioner enzyme that consumes neuronal NAD+ during axon injury, reframing NAD+ as the molecular switch between axon survival and programmed degeneration.
Matrikines are peptide fragments released when the extracellular matrix breaks down, and they act as endogenous signals telling fibroblasts to rebuild collagen, elastin, and hyaluronic acid. Topical peptides like Matrixyl and GHK-Cu are essentially exogenous mimics of this repair cascade.
SIRT3 is the principal NAD+-dependent deacetylase inside mitochondria, controlling oxidative defense, fatty acid oxidation, and proteostasis. Its decline with age links falling NAD+ pools directly to mitochondrial dysfunction.
SIRT3 is the principal NAD+-dependent deacetylase inside mitochondria, controlling oxidative defense, fatty acid oxidation, and proteostasis. Its decline with age links falling NAD+ pools directly to mitochondrial dysfunction.
PQQ is a redox-cycling cofactor that activates CREB and PGC-1α, the master regulator of mitochondrial biogenesis. Unlike CoQ10, PQQ stimulates the formation of entirely new mitochondria.
Matrikines are bioactive peptide fragments released from degraded extracellular matrix proteins. They act as molecular distress signals that reprogram fibroblasts toward repair — explaining why tripeptides like GHK and palmitoyl-pentapeptides outperform conventional skincare actives.
MMP-1 and MMP-2 dysregulation — not declining fibroblast output — is the primary driver of dermal aging. TIMP rebalancing and copper-dependent enzymatic control restore ECM homeostasis.
Matrikines are bioactive peptide fragments released during extracellular matrix turnover that act as feedback signals to fibroblasts. GHK-Cu is the archetypal example, driving collagen synthesis and skin remodeling.
NMN raises NAD+ — but where it raises it depends on the delivery route. The Slc12a8 transporter controversy and route-dependent pharmacokinetics explain why brain, muscle, and liver respond differently.
Urolithin A is a gut microbiome-derived metabolite that activates mitophagy through the PINK1/Parkin pathway. Only 40% of adults produce it from dietary ellagitannins, making direct supplementation clinically relevant for mitochondrial health.