Over at the SENS Foundation, you'll find fairly detailed commentary from Michael Rae on the recent news of progress towards a viable therapy for the rare accelerated aging condition progeria. As I've noted in recent years, one of the things learned about the mechanisms of progeria is that they seem to be a greatly exaggerated version of processes that happen in all of us - in the same sense that the runaway mechanisms of Alzheimer's or Parkinson's disease (and many other age-related conditions) take place at low levels in all of us.
So should we do more than keep a weather eye on progeria research? Probably not:
All of us at SENS Research Foundation are inspired by the rapid progress that was made against this tragic disease ... However, it is also important not to read too much into this apparent advance in regards to its implications for the development of new medicines against the diseases and disabilities of aging. In particular, the common characterization of HGPS "progeria" as a disease of "premature aging" leads some to expect that this research has direct implications for the development of rejuvenation biotechnologies, targeting the damage and disabilities of aging.
It is true that the splicing defect responsible for formation of progerin is sporadically active in wild-type cells, and that number of cells in which progerin is present and the level at which it appears do appear to rise with aging. However, such cells are rare enough, and their progerin levels low enough, as to seem highly unlikely to meaningfully contribute to tissue dysfunction with aging, at least within the bounds of a currently-normal lifespan. Additionally, there is evidence that progerin can be turned over in the nuclear lamina, and the causal relationship between the higher prevalence of progerin in aging cells and cellular senescence or disease are not clear, leaving open the possiblity that repair of well-established forms of aging damage may in turn lead to the reversal or obviation of this phenomenon.
Notably, the need to remove "senescent" cells as part of a comprehensive panel of rejuvenation biotechnologies is already clear from first principles, and its potential to ameliorate aspects the frailty and disability of aging has been demonstrated in proof-of-concept rejuvenation research, rendering the specific role of progerin in the process moot. That is, removing "senescent" cells is essential whether progerin accumulation is a cause or a consequence of cellular senescence, and will be equally effective as a regenerative medical therapy against age-related disability in either case.
It is absolutely the case that we'd expect new and interesting challenges to show up once people are living well past the normal human life span. We'd expect to see forms of biological damage that are generally irrelevant over the course of a century turn out to be lethal at two centuries, for example - perhaps nuclear DNA damage, perhaps progerin accumulation, perhaps the fact that some important macromolecules are never normally replaced, perhaps more obscure aggregated metabolic waste products. So largely things we presently know about, can presently ignore, and will have a great deal of time to work on should it turn out to be problem down the line.