I listened to your piece and you sounded very good – I like your approach and I didn’t miss that plasma exchange came first on your list of “flagship” projects – as well it should. There’s hardly any field of research that is more suited to humans than to animals; the existing equipment for plasmapheresis and plasma exchange is made, (and medically approved), for humans and not animals (though it might be okay for large dogs, pigs, etc.).
As the only approach demonstrated to reverse aging, in situ, in living animals, without requiring genetic engineering, nor requiring any technological break-through whatsoever – with admittedly only ‘circumstantial evidence – and (Edouard) some contradictory evidence that is minimally relevant (as the procedures will differ enormously). – but it is the gamble ( a relatively cheap one, according to how rich you are).
There are still some technical questions that need to be asked – as for example; are there effective means of storing plasma/serum long-term? But of course the biggie will be the biomarkers; I think I’ve picked appropriate ones – as those which are the most conservative according to a paper by the most conservative of critics of programmed aging, Tom Kirkwood. So while telomere length would be a nice thing, there’s no good correlation among 85+year old’s life expectancy and telomere length. Some cruder criteria like total hemoglobin concentration are called for. I would really like to see DNA and epigenetic studies of rejuvenated cells, and we can see if we can get some cooperation with people doing that work (money talks). In humans you can judge age relatively, and in the only way that matters, by peoples appearance – a trait that we’re not adept at judging in animals so we should use that. We also would want to study the chronic inflammation associated with aging, following the standard biomarkers in the blood – like CRP (‘c-reactive protein) etc An interesting question I think was made by Amy Wagers about GDF11 not ‘de-aging’ the body but repairing it. I believe Amy belongs to the ‘wear and tear’ school of aging which likes aging cells to damaged cells – so by that definition, what is the difference between repairing cells and ‘de-aging’ them? – if aging is damage, then ‘de-aging’ would be the repair of damage. Truth is that you can ‘de-age’ cells – you can de-age nuclei (‘rejuvenate’ is a better term) by inducing them to pleuripotence – using transcription factors or even small molecules). and that changes their age phenotype – even changing their telomere lengths and transcription patterns (obviously), making their mitochondria efficient, producing more ATP and fewer ROS. Evidence is that organs transplanted serially can last multiples of their original lifespans – and knowing that a thymus can go back to functionality after involution guarantees that age-phenotype at the organ level is controlled by the plasma; that it can last the life of a new host after being brought back signals another lifespan at least (if you wait until you’re old). But if it’s true – then the young could benefit even more- there’s no better way (that I can think of) of avoiding the diseases of aging than by not aging. Well we’ll see.