Researcher Michael Rose has interesting views on aging and longevity that diverge from much of the rest of the present research community. He is possibly best known for his work showing a late-life mortality plateau in flies - if you define aging as a rising risk of death per unit time, then there is very clearly a point at which aging stops in that species. Mortality is still high and the flies still die, but for a while they are what Rose terms "immortal," a term he adopts to mean no further rise in mortality rate. So far the data is either ambiguous or in opposition to the existence of a mortality plateau in humans, however.
My work on the evolution of aging in response to changes in the first age of reproduction has been emulated with mice by Nagai, Lin, and Sabour (1995, Growth Dev Aging), who showed that you get the same qualitative results with rodents as with flies. This and other experiments manipulating the timing of reproduction in other species show that Hamilton's 1966 Forces of Natural Selection are the fundamental controls on aging. As for the full range of experiments in the Rose and Mueller labs on the evolution and cessation of aging, no one else has come up with such a complete range of experiments to test the hypothesis that Hamiltonian theory explains the onset, rate, and cessation of aging.
Hamilton's forces start to fall after the start of reproduction, which is when aging starts. But Hamilton's forces eventually stop falling at late adult ages. If aging only occurs during or a bit after these forces are falling, then aging must eventually stop too. This means that mortality rates, fertility, and virility should all eventually reach plateaus at which they change only gradually. That is what we have found in our lab data with fruit flies.
SENS and most other thinking about aging is dominated by the hypothesis originally due to Aristotle that aging is produced by some type of physiological process, whether that process involves damage or a death program. In Hamiltonian thinking, aging is the de-tuning of adaptation during the first part of adulthood. As such, we see aging as a problem as complicated as that of evolutionary adaptation itself. Thus we expect that aging is due to many problematic nucleotide frequencies, distributed genome-wide, which in turn generate pleiotropic and epistatic effects of great complexity throughout the biology of aging organisms.