The interaction between medical technology and specific biological mechanisms determines limits to human life span. Given the sparse nature of demographic data

The interaction between medical technology and specific biological mechanisms determines limits to human life span. Given the sparse nature of demographic data for extreme old age, there is plenty of room to debate whether or not there exists one or more mechanisms of aging that have not been impacted in any meaningful way by improvements in medical technology over the past century, and which, on their own, can produce a very high rate of mortality in late life. That circumstance would look a lot like a limit to human life span, one that doesn't appear to be affected by medicine - but that is only because the right medicine hasn't been created yet. One mechanism that springs to mind here is the accumulation of transthyretin amyloid, found in one small study to be the majority cause of death in supercentenarians, but which appears to have only a smaller impact on mortality in younger old age - it is implicated in something like 10% of heart failure cases, for example. Can we argue that advances in medicine and public health over the past century have had little to no impact on the accumulation of misfolded transthyretin deposits in tissues, and thus this mechanism acts as a limit on life span? Or do some of these improvements in fact produce an small, incidental reduction in amyloid burden in later life? The evidence to support any of the possible positions on these questions is presently lacking. Whatever the state of effective limits on life span today, however, the limits on life span tomorrow are determined by progress towards rejuvenation therapies. There are treatments under development that can clear transthyretin amyloid from tissues, for example, such as the work of Pentraxin Therapeutics, or the catalytic antibody development funded by the SENS Research Foundation.