Telomere Rivers: Rejuvenation And Lifespan Extension

Added: 2026-05-12

[00:00:00]We take these readers. These readers can be transplanted into other old animals and these readers trigger life extension. These can be done through the readers, they can be done by adoptive transfer of the dose T cells. It can be done through the GAB 1 H depletion of the artificial readers. I think some people have commented on the background controls and the mortality. Yes, there are some background controls dying earlier 30% to my eye. And people should focus on the fact on the divergence at the point of the interventions, which is 20 months. At 20 months, there is this divergence even if you exclude background mortality, you still have the life extension. In the siRNA control versus siRNA GAB 1 H where you do not see this background mortality, you still have this life extension. So, I think people should engage with the data looking at the data for what they are. I anticipate we have other controls that have intact mortality up to 20 months and there is still the same result. We just wanted to show the data that we had at the time pre-print. In the final paper, there will be further controls, but the controls the background mortality before the intervention had nothing to do with the intervention per se. The individual dots are not individual animals. This is what prism look like and the animals are what we show figure legends of the pre-print. We will have more controls, but I wanted to answer this because I had seen, you know, some comments about it and I was quite uh surprised about it. So, I guess and I hope this will serve to satisfy them.

[00:01:46]So, our model telomere regeneration is quite simple when we strip off all the noise. We have a T cell and we have an antigen presenting cell. When the T cell engage on fatty acid oxidation, it can cluster through ceramidase activation. It can cluster the C3 on the bullae of the synapse and this trigger telomere transfer from the APC. The telomere transfer from the APC proceeds with a short MCD, the greater sheltering, includes T zap and so on through a calcium flux in the APC. These vesicles contain RAD51 and once these lands into the T cell, there's two things that happens.

[00:02:30]It extends telomeres ultra short telomeres in the T cells that undergo stem-like switch and upon stem-like switch in early life division, one of the two daughter cell CPT1A bright cell readers that are depleted of GAB 1 H because the cell itself has, you know, somehow reduced the GAB 1 H tone of the of the of the daughter cell, right? So, you have this stem-like T cell that within the first division releases these readers. After the subsequent divisions, these capacities are now lost. We have another paper in revision in Nature, so I can't say much about this, but there are some T cells that are hyper proliferating and that have evolved these unique capacity to produce these readers and to keep us fit. And the overall outcome is systemic rejuvenation, increase of stem-like signaling and extraordinary life extension. Something also that I think we should train ourselves in thinking is that if you think about the gain we get through telomere transfer, which is roughly 30 times what you get through atelomerase activation, it sounds surprisingly matches incredibly the gain that we have observed in our life extension studies, roughly 20-30 times more than what in general in the longevity space you observed by turning telomerase or buying rapamycin or mTOR inhibition.