Longevity
Compounds and mechanisms studied for slowing cellular aging — NMN, resveratrol, autophagy.
4.1NMN (Nicotinamide Mononucleotide)
An NAD+ precursor intensively studied in the context of cellular aging — human data are still early, despite huge market popularity.
3.9Resveratrol
The red-grape polyphenol famed as a 'sirtuin activator' — but its bioavailability in humans is very low, which limits the practical relevance of many striking test-tube results.
4.3Autophagy
An intracellular 'housekeeping' process that clears out damaged proteins and organelles, whose discovery earned a Nobel Prize — one of the key mechanisms studied in the context of slowing aging.
4.4Telomeres and Telomerase
Protective 'caps' on the ends of chromosomes that shorten with every cell division — one of the most recognizable, though still imperfect, biomarkers of cellular aging.
4.05-AVAB
5-aminovaleric acid betaine (5-AVAB) is a small molecule produced by the gut bacterium Bifidobacterium pseudocatenulatum, whose levels decline with age — in mice, giving it reduced age-related inflammation and improved cognitive and motor function.
3.9Urolithin C
Urolithin C is one of the lesser-known metabolites from the same family as the well-studied urolithin A — it forms from the same plant compounds, but in cell and animal studies it stands out with a different activity profile, including in the context of insulin secretion.
3.8Urolithin D
Urolithin D is the least-characterized but, in cell-based studies, the most potently antioxidant member of the urolithin family — compounds produced by gut bacteria from ellagitannins found in pomegranates, walnuts, and other foods.
4.1Proteostasis
A cell's ability to maintain balance between protein production, correct folding, and degradation — a network of mechanisms whose capacity declines with age and is studied as one of the fundamental pillars of cellular aging.
4.0UPRmt
The mitochondrial unfolded protein response (UPRmt) is an intracellular repair program that protects mitochondria from stress — linked to lifespan extension in model organisms, though the relationship turned out to be more complex than initially thought.
4.2TFEB
The transcription factor TFEB acts as a master on-off switch for autophagy and the production of new lysosomes in the cell — one of the best-characterized molecular nodes linking these two processes, studied as a potential target for interventions in aging.
3.9Lysosomal Health
Lysosomes — the cell's 'recycling centers' — accumulate unprocessed waste and lose capacity with age, a pattern increasingly described as one of the fundamental, shared denominators of cellular aging and a potential target for future interventions.
4.0Mitophagy
A selective form of autophagy in which the cell recognizes and removes specifically damaged, dysfunctional mitochondria — a mitochondrial quality-control mechanism whose efficiency declines with age and is studied in the context of neurodegenerative disease.
4.2Immunosenescence
The progressive, multi-directional remodeling of the immune system with age — not a simple 'weakening,' but a complex change that both lowers the ability to fight new threats and raises the baseline level of inflammation.
4.3Inflammaging
Chronic, low-grade, systemic inflammation that accompanies aging even without an active infection — a term coined in 2000 by Claudio Franceschi, today considered one of the fundamental mechanisms linking aging to age-related disease.
4.2NAD+ Recycling
The level of NAD+ in the body isn't just about how much of the coenzyme a cell makes from scratch — it's mainly about how efficiently it reclaims NAD+ from the byproducts of its own breakdown, a process called the salvage pathway, whose efficiency declines with age regardless of how much precursor is supplied through diet or supplements.