Questions and answers submitted to the SENSible blog.
A supporter asks: Everyone knows that mitochondrial free radicals are a key driver of aging, and antioxidants don’t seem to offer any protection. Birds are supposed to have very clean-burning mitochondria, so should you maybe try to cut them off at the source by re-engineering our mitochondria to be more like those of birds?
A supporter asks if “backing up” copies of the mitochondrially-encoded genes in the nucleus is really viable, granted free radical damage in the nucleus. We emphasize the many additional ways that the nuclear copies will be safer than the mitochondrial originals, that the “backup copies” can be backed up again, and how they and additional strategies will buy us time for even better solutions.
An article criticizes the diagnosis of Alzheimer’s in its earliest stages based on the presence of beta-amyloid or other aging damage in the brain and read this post to understand why this critique may be unfounded.
A supporter asks if the Hallmarks of Aging could effectively be substituted for the seven categories of cellular and molecular damage in the SENS platform. The answer is ‘no,’ because the Hallmarks include both too much and too little, and most importantly because the Hallmarks fail to serve as a roadmap toward the biomedical postponement of aging.
A supporter asks if the Hallmarks of Aging could effectively be substituted for the seven categories of cellular and molecular damage in the SENS platform. The answer is ‘no,’ because the Hallmarks include both too much and too little, and most importantly because the Hallmarks fail to serve as a roadmap toward the biomedical postponement of aging.
Skeletal muscles are organized into long fibers, and when a fiber breaks the entire fiber is often lost. This made a supporter worry that senolytic therapies might break a muscle fiber and eliminate precious fibers in aging muscles. It appears that the injury at the heart of the questioner’s worry does not happen in practice.
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?
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