Featured posts for SRF News and where featured posts should appear.
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.
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.
In a groundbreaking announcement set to impact the future of longevity research and outreach, two historic longevity nonprofits —SENS Research Foundation and Lifespan.io (Lifespan Extension Advocacy Foundation)—have unveiled plans to merge, upon completion of regulatory approvals.
Sign up to stay informed about the latest news and opportunities with SRF!
Use of this Web site constitutes acceptance of the Terms of Use and Privacy Policy.
© 2024 SENS Research Foundation – ALL RIGHTS RESERVED
Sign up to stay informed about the latest news and opportunities with SRF!
Use of this Web site constitutes acceptance of the Terms of Use and Privacy Policy.
© 2024 SENS Research Foundation – ALL RIGHTS RESERVED
