Michael Rae 
Metformin has been proposed as an “anti-aging drug,” and scientists are organizing TAME, a major clinical trial to test the idea. In Part 1 of this 5-part series, we look at the animal studies underlying this idea.
A supporter asks if SENS rejuvenation biotechnologies will benefit patients with progerias — so-called “premature aging” diseases.
Some scientists have reported that viruses, bacteria, and other pathogens may help drive Alzheimer’s and other neurodegenerative diseases, and that the body uses beta-amyloid protein to fight them off. That seems to imply that it’s a bad idea to remove Abeta from the brain. Here we explain how the SENS “damage-repair” strategy leaps over that therapeutic dilemma — just as it does with other kinds of aging damage.
For our SENSible Question series, a supporter asks if there are any common lab tests available that could be used as a readout of a person’s burden of inflammatory signals from senescent cells. The answer is ‘no,’ unfortunately, but we review a number of hard-to-access or research-only tests that might be able to tell us something with a bit more work.
We are proud to announce the recent publication by Sharma lab/ApoptoSENS team in the journal Aging describing an improved method for enriching primary NK cells from human peripheral blood and demonstrating the ability of those NK cells to eliminate senescent cells by recapitulating more physiological conditions and potential therapeutic interventions.
We are proud to announce the recent publication by Sharma lab/ApoptoSENS team in the journal Cells describing the role and controversies involving the aging of Natural Killer (NK) cells and age-related NK cell dysfunction. This review focuses on recent advances and open questions in understanding the interplay between systemic inflammation, senescence burden, and NK cell dysfunction in the context of aging and potential therapies for age-related diseases.
SENS Research Foundation’s science writer Michael Rae was interviewed on the Parkinson’s Recovery radio program on “The coming rejuvenation biotechnology revolution for Parkinson’s disease.” In it, they discussed how the cellular and molecular damage of aging most closely involved in Parkinson’s can be removed, replaced, or repaired using rejuvenation biotechnologies, and research underway to make it happen. Read more and listen to the interview to learn how a “damage-repair” approach can prevent, arrest, and eventually consign Parkinson’s to history.
Lower-quality, clickbait-hungry media outlets love sensationalist claims, but one does expect better from the public relations department of an internationally-respected research university. And it was an easy jump from the already-overstated “In First, Aging Stopped in Humans” and “treatments can reverse two processes associated with aging and its illnesses” to saying that a treatment “can reverse …
In heterochronic parabiosis, joining the circulatory systems of young and old mice causes the older animal to recover some features of youth. The effect has been widely assumed to be driven by pro-youth factors in younger blood, but an alternative hypothesis is possible: that the procedure is instead diluting pro-aging factors in the older partner.
Q: When senolytic drugs cause senescent cells to die, other (younger) cells need to divide and take the place of the dead cells. This cell division causes telomere shortening, thus possibly creating new senescent cells. How is it that the process of killing senescent cells is not self-defeating if new senescent cells are being created? …
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© 2025 SENS Research Foundation – ALL RIGHTS RESERVED
