Michael Rae 
Mitochondrial free radicals play a crucial role in aging, and despite efforts to use antioxidants, mammals haven’t significantly extended their lifespans. Birds, known for their clean-burning mitochondria, raise an intriguing question: Should we engineer our mitochondria to be more like theirs?
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.
Aging muscles lose strength above and beyond what would be expected from the mere loss of muscle mass. Accordingly, many drugs have been shown to stimulate muscle growth in older people, but the increased muscle mass consistently fails to translate into increased strength and physical function. To let people live independent lives for longer, we need damage-repair longevity therapeutics to repair the cellular and molecular damage that makes aging muscle dysfunctional.
Several pharma companies are currently running clinical trials on damage-repair therapies targeting damaged forms of the protein tau to combat Alzheimer’s disease. But these AmyloSENS therapies only reach tau in the fluid outside of neurons, when what we need is to clear damaged tau inside of them. Fortunately, researchers are beginning to use mRNA — the same revolutionary biotechnology platform of the best COVID vaccines — to develop new LysoSENS therapies to do just that.
A recent preprint reports that use of Viagra and related drugs is associated with a lower mortality rate, raising hopes that it might be repurposed as a longevity therapeutic. Unfortunately, the methodology used in this and other recent studies is too weak to arouse too much excitement just yet.
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.
How SENS “damage-repair” longevity therapeutics can prevent and reverse the second most common neurodegenerative disease: neurodegenerative aging of the Parkinson’s type.
The Phase III trials for AmyloSENS rejuvenation biotechnologies lecanemab/Leqembi® and donanemab showed that they are most effective when given to people with less of other kinds of cellular and molecular aging damage in their brains. New data illustrates that fact even more powerfully and gives us a foreshadowing of what’s possible if we make best use of these and forthcoming damage-repair longevity therapeutics.
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.
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© 2024 SENS Research Foundation – ALL RIGHTS RESERVED
