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.
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.
Matrikines are peptide fragments liberated when collagen and elastin break down — and they act as feedback signals telling fibroblasts to rebuild the extracellular matrix.
Matrix metalloproteinases MMP-1, MMP-2, and MMP-9 are the primary enzymes responsible for collagen destruction in photoaged skin. Understanding their UV-driven upregulation and TIMP-mediated counter-regulation reveals the molecular basis of dermal aging.
NMN faces a pharmacokinetic paradox: it raises NAD+ in tissues even though most oral doses are degraded before absorption. Understanding the Slc12a8 transporter and the NMN-to-NR-to-NMN cycle explains why delivery route fundamentally shapes outcomes.
Decorin is the small leucine-rich proteoglycan that dictates collagen fiber diameter, spacing, and tensile behavior in skin — controlling dermal architecture far more than collagen quantity alone.
Decorin is the unsung architect of dermal collagen — regulating fibril diameter, binding TGF-β, and modulating repair. Its loss with photoaging reframes skin aging as a proteoglycan deficit, not merely collagen depletion.
The Na+/K+-ATPase consumes nearly a third of the body's resting energy budget to maintain the ion gradients that make life possible. Its decline drives neuronal hyperexcitability, arrhythmia, and cognitive aging.
CD38 is the dominant consumer of NAD+ in aging tissues, and its activity rises sharply with inflammaging and senescent cell accumulation — making it a central enzymatic axis linking metabolic decline to cellular aging.
PGC-1α is the transcriptional coactivator that builds mitochondria, enables oxidative metabolism, and powers brown fat thermogenesis. Its age-related decline is a central driver of metabolic inflexibility.