Scientific Glossary

Inflammaging (portmanteau of inflammation + aging) describes the chronic, sterile, low-grade inflammatory state that characterizes aging. Driven by senescent cells (SASP), mitochondrial dysfunction, gut dysbiosis, and accumulated cellular damage. Associated with increased IL-6, TNF-α, CRP, and other inflammatory markers. Most age-related diseases (cardiovascular, metabolic, neurological, cancer) share inflammaging as a common driver. Anti-inflammatory peptides studied for longevity include KPV, ARA-290, and thymosin alpha-1.

Acute inflammation (redness, heat, swelling, pain) is a protective cascade involving vasodilation, immune cell recruitment, and cytokine release. It clears pathogens and damaged tissue, enabling repair. Chronic inflammation is pathological — sustained cytokine production damages healthy tissue and drives metabolic disease, cardiovascular disease, neurodegeneration, and cancer. Many research peptides are studied for anti-inflammatory properties: KPV (IL-1beta antagonism), BPC-157 (NF-κB modulation), ARA-290 (innate repair receptor), thymalin, and TB-500.

Neuroprotective strategies include antioxidant defense, anti-inflammatory actions, neurotrophic factor support (BDNF, NGF), mitochondrial protection, and excitotoxicity prevention. Research peptides studied for neuroprotective properties include: Semax (increases BDNF, studied in stroke recovery), Selank (anxiolytic, studied in PTSD models), Pinealon (from Russian neuroprotection research), Dihexa (NGF-potentiating hexapeptide), and MOTS-c (mitochondrial protection in neuronal models). The blood-brain barrier presents the primary challenge for CNS-targeted peptide delivery.

NMN is phosphorylated to NMN-dinucleotide (NMND) and then to NAD+ inside cells. As a direct precursor, NMN can raise NAD+ faster than more distal precursors like tryptophan. Human trials have demonstrated that oral NMN supplementation significantly elevates NAD+ metabolites in blood and muscle tissue. Japanese RCT (Igarashi 2022): 250mg/day NMN improved muscle insulin sensitivity and physical performance metrics in older adults. Note: NMN vs. NR (nicotinamide riboside) comparative research is ongoing.

Sirtuins require NAD+ as a cosubstrate to function, linking cellular energy status to epigenetic regulation. SIRT1 activates PGC-1α (mitochondrial biogenesis), FOXO transcription factors (stress resistance), and p53 (DNA repair). SIRT3 maintains mitochondrial function. SIRT6 is essential for DNA double-strand break repair and telomere maintenance. Declining NAD+ with age reduces sirtuin activity, contributing to the aging phenotype. NAD+ precursor supplementation research aims to restore sirtuin activity as a longevity intervention.

Telomeres are repetitive DNA sequences (TTAGGG) that protect chromosome ends from degradation. Each cell division shortens telomeres slightly. When telomeres become critically short, cells enter senescence or apoptosis. Telomere length is associated with biological aging — shorter telomeres correlate with age-related disease risk in epidemiological studies. Epithalon and other peptides are studied for potential telomerase-activating properties that might theoretically slow telomere shortening.