Most living things age. Cells accumulate damage, tissues lose function, and the risk of death rises with time. Yet a handful of species appear to escape this pattern, and researchers are studying both those natural exceptions and the molecular machinery of aging in the hope of extending healthy human life.True biological immortality—the absence of aging as a cause of death—is rare. The best-known example is the small jellyfish *Turritopsis dohrnii*. When injured, starved, or stressed, the adult medusa can transform back into a juvenile polyp and begin its life cycle again. In laboratory conditions this reversal has been observed repeatedly. The animal is still vulnerable to predators and disease, so individual jellyfish do not live forever in the wild. The ability to reset its developmental clock, however, makes it a striking model of cellular plasticity.Other organisms show negligible senescence: their chance of dying does not increase markedly with age. Certain turtles, some fish, and the freshwater polyp *Hydra* maintain stable physiological function for decades or longer. These cases demonstrate that aging is not an inevitable law of biology but a process that evolution has modulated in different ways.How Aging Works in HumansIn people, aging is driven by multiple overlapping mechanisms. DNA damage and mutations accumulate. Telomeres—the protective caps on chromosomes—shorten. Proteins misfold. Senescent “zombie” cells build up and secrete inflammatory signals. Mitochondria lose efficiency. Epigenetic marks that control gene activity drift away from their youthful patterns. Immune function declines. The result is the familiar rise in chronic disease and frailty.Some researchers view aging primarily as the accumulation of random damage. Others see elements of a more programmed process, with coordinated shifts in cell populations and gene regulation across tissues. Both perspectives guide current intervention strategies.Paths Toward InterventionSeveral approaches are under active investigation.Senolytics aim to clear senescent cells. In animal studies, removing these cells can improve tissue function and extend healthspan. Early human trials are testing related compounds for specific age-related conditions.Partial cellular reprogramming uses a subset of the Yamanaka factors—genes that can return adult cells to a more youthful state—without fully erasing cell identity. In mice and some non-human primates, controlled reprogramming has reversed aspects of aging in tissues. The first carefully designed human trials of related gene therapies have begun, initially focused on eye diseases where local delivery is safer.Other avenues include drugs that mimic calorie restriction (such as rapamycin and its analogs), therapies that support stem-cell populations, efforts to improve DNA repair, and epigenetic resetting. Combination approaches are also being tested in animals, on the theory that aging’s multiple causes may require multiple simultaneous repairs.Realistic HorizonsNo therapy has yet produced biological immortality in humans, and none is close. Mathematical models that assume all reversible aging processes could be eliminated still leave a residual limit set by irreversible mutations in long-lived cells such as neurons, suggesting theoretical ceilings in the range of roughly 150 years under optimistic assumptions. Reaching even that point would require solutions that do not currently exist.Near-term progress is more likely to appear as extended healthspan—more years free of disability—rather than radical lifespan extension. Clinical trials are moving from mice into humans for several interventions. Regulatory pathways for treating aging itself, rather than individual diseases, remain under discussion.The “immortal jellyfish” and other long-lived species prove that biology can solve the problem of senescence in principle. Translating those solutions, or engineering new ones, into safe and effective human therapies is a far harder task. Research is accelerating, funding has increased, and the first controlled human experiments in cellular rejuvenation are under way. Whether these efforts ultimately add decades of healthy life, or merely modest improvements, will be answered by data still being gathered.