Topic: Biological Age Locks.
Basically, there's a biological cap on age here.
The Hayflick limit[Note 1] (or Hayflick phenomenon) is the number of times a normal human cell population will divide until cell division stops. Empirical evidence shows that the telomeres associated with each cell's DNA will get slightly shorter with each new cell division until they shorten to a critical length.
Now there's work being done to deal with this issue.
Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced staining for β-galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine.
Here in mice we have actual reversal of aging:
The Harvard team that published that said:
Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease risk1, 3 and the marked reversal of systemic degenerative phenotypes in adult mice observed here support the development of regenerative strategies designed to restore telomere integrity.
Now of course these things are all far from understood, but we're gaining some headway in these areas. That's only a single bio-marker, however, and there are many more natural caps to be overcome to extend aging. Not all of which even need to be totally understood for them to work.
Here we have hamsters who scientists severed the optic nerve of leaving them blind, and what they did was build peptide based tiny "nano" particles, made a cut, injected them, and they bridged the gap of the severed nerve, allowing the nerve to effectively regrow and allow for sight to function again. That's already a thing.
There's also these girls who seemingly age extremely slow:
Like infants but getting on to 10 years old or so. No discernible aging.
Idk I think we'll probably solve aging in the next 200 years. If not biologically perhaps technologically. I think most of us will hit at least 120 age-wise.