A supporter raises a new angle on an old concern: might fabulously wealthy people hoard longevity therapeutics for themselves? The context for the question and the motivation behind it are different, but the answer is still “no.” Rejuvenation biotechnology will be widely available to aging people, and SENS Research Foundation will work at the front end and the back end to ensure that access to longevity therapeutics expands as quickly and as widely as possible.
A supporter asks us to compare the expected benefits of Cyclarity’s UDP-003 to chelation therapy. Although both target the age-related scourge of atherosclerotic cardiovascular disease (ASCVD), EDTA (if it works) dampens down the worst aspects of having ASCVD, while UPD-003 is a SENS “damage-repair” therapeutic which is expected to remove the underlying damage itself and reverse the disease process.
A supporter asks us if it would accelerate research progress much faster if did most testing in far shorter-lived animals, like the roundworm C. elegans or the fruit fly Drosophila – rather than mice.
A supporter asks us to elaborate on projects other than allotopic expression (AE), that SRF has undertaken that are targeting mitochondrial dysfunction; and how they relate to the original strategy of allotopic expression?
A supporter asks about the investigative report in Science magazine that suggests the critical study identifying beta-amyloid oligomers as the key actors in Alzheimer’s disease may have been based on fraudulent data.
A supporter asks about how the central MitoSENS strategy can be delivered to our cells.
A supporter asks if cellular reprogramming turns an old person’s cells young again,can’t we fix aging by just reprogramming a person’s old cells with reprogramming factors?
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.