Questions and answers submitted to the SENSible blog.
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.
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