Our Blog discusses the development of rejuvenation biotechnology around the world: progress being made in the field of longevity, the design of medical therapies to cure, reverse and prevent the diseases and disabilities of aging, and much more.
Our content is a blend of popular interest articles – labelled “Easy Reads”, and designed to require no specific background knowledge – as well as more detailed scientific commentaries, labelled as “In-Depth” and aimed towards readers with some grounding in the biological/medical sciences.
Aberrant tau inside neurons is a key driver of Alzheimer’s disease, but nearly all the therapies in development to target it can only capture the small amount that floats outside of them. A new animal study reports impressive results in clearing aberrant tau inside neurons and rejuvenating cognitive function, opening up an important new front in damage-repair strategies for maintaining the aging brain.
A recent study claimed to find that metformin rejuvenated cognitive function in aging monkeys and lowered biological age on a nonhuman primate biological age clock. The details make the result unconvincing.
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.
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