This piece of the puzzle, and its finding, if confirmed, is very neat. But I think we are barking at the wrong tree, because senescence is inherently chaotic. Sometimes we identify a disease with a set of common symptoms because there are many alternative causes that lead to those very symptoms. It's like "convergent symptoms", so to speak.
If I had any funding to work freely in these subjects, I would instead focus on the more fundamental questions of computationally mapping and reversing cellular senescence, starting with something tiny and trivial (but perhaps not tiny nor trivial enough) like a rotifer. My focus wouldn't be the biologists' "we want to understand this rotifer", "or we want to understand senescence", but more "can we create an exact computational framework to map senescence, a framework which can be extended and applied to other organisms"?
Sadly, funding for science is a lost cause, because even where/when it is available, it comes with all sort of political and ideological chains.
If I had any funding to work freely in these subjects, I would instead focus on the more fundamental questions of computationally mapping and reversing cellular senescence, starting with something tiny and trivial (but perhaps not tiny nor trivial enough) like a rotifer. My focus wouldn't be the biologists' "we want to understand this rotifer", "or we want to understand senescence", but more "can we create an exact computational framework to map senescence, a framework which can be extended and applied to other organisms"?
Sadly, funding for science is a lost cause, because even where/when it is available, it comes with all sort of political and ideological chains.