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.
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.
Another clinical trial has now proven that a second AmyloSENS rejuvenation biotechnology that clears beta-amyloid aggregates from the brain also slows down the slide into dementia in people in the early stages of Alzheimer’s disease, but this development is only the beginning.
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.
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© 2024 SENS Research Foundation – ALL RIGHTS RESERVED
