SENS Research Foundation and Lifespan.io Announce Intent to Merge, Forming a Novel Longevity Entity MOUNTAIN VIEW, April 3, 2024 – 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. Lifespan.io, renowned for its unwavering advocacy for longevity and responsible journalism, is joining hands with SENS Research Foundation, a trailblazer in longevity-focused resea ..read more

The Problem Senescent, or old, cells drive diseases of aging in tissues far removed from where the damaged cells are located. It is assumed that these effects result from factors that senescent cells release (the “SASP”) being carried by the blood, but this hasn’t been proven in studies. If senescent cells don’t raise the level of SASP in blood, it’s unknown how they cause the damaging effects of aged blood or explain the whole-body benefits when senescent cells are removed. The Goal Looking at how the SASP has been defined – as mostly proteins that don’t correlate well to the volume of senesc ..read more

The Problem IPF is linked to the accumulation of senescent, or old, cells in the lung, creating scar tissue (fibrosis) which progressively stiffens them. This disables the patient, eventually suffocating them within 2-4 years. IPF creates a high burden of senescent cells in the lungs, and removing senescent cells powerfully impacts the disease. Previous drug candidates were tested in a problematic model which doesn’t accurately reflect the reality of IPF patients, whose pathology accumulates over many years in lungs that have limited capacity to heal. The Goal Develop a new and more reliable m ..read more

The Problem The immune system has an ability to patrol for and destroy senescent, or aged cells, a function which deteriorates over time, permitting senescent cells to accumulate and drive age-related disease. The negative impacts from senescence may actually result from a joint attack by both senescent cells and activated macrophages – a type of immune cell. These cells can be mistaken for senescent cells, as they are present in aged tissues and have some of the same identifiers.  The Goal Using specific senolytics – or drugs that remove senescent cells – to eliminate both senescent cell ..read more

The Problem The immune system can patrol for and destroy senescent, or aged cells. Senescent cells are drivers of age-related disease and removing them helps remediate aged tissues. It was recently discovered that these cells have an unusually high metabolism.   The Goal Reduce the metabolism in the senescent cells to see if doing so renders them non-functional. Drugs currently on market have this ability but were developed for an unrelated purpose and were ultimately abandoned. We aim to harness them in the fight against senescence as a new type of senolytic – or drug that kills senescen ..read more

The Problem The immune system, including natural killer cells (NK cells), has an ability to patrol for and destroy senescent, or aged cells. However, this protective function deteriorates over time, permitting senescent cells to accumulate in our tissues and drive age-related disease. Drugs used to destroy senescent cells – senolytics – use a brute-force method that can disrupt natural function. The immune system clears out the aged cells at the best time, in the best way, allowing for natural function. The Goal Using CAR technology designed for cancer treatment, our team is engineering NK cel ..read more

The Problem Aging creates an accumulation of mutations in the DNA of our mitochondria, the organelles that create our energy supply on a molecular level. This impacts and impairs their ability to function correctly and creates a myriad of energy issues as we age. Testing potential therapies for use in humans requires a robust testing model that hasn’t yet been developed.  The Goal Building upon a prior SRF program, the team engineered mice that have specific mutations in their mitochondrial DNA. They grow normally but show the defects common in humans with the same types of mutations.&nbs ..read more

The Problem Aging creates an accumulation of mutations in the DNA of our mitochondria, the organelles that create our energy supply on a molecular level. This impacts and impairs their ability to function correctly and creates a myriad of energy issues as we age.  The Goal The team is creating a drive to implant new genes more aggressively, like a sped-up evolutionary track, through mitochondria that have been engineered with an enzyme capable of destroying all current mitochondrial DNA in a cell. These new mitochondria will replace all the mutated and aged mitochondria with healthy, func ..read more

The Problem Aging creates an accumulation of mutations in the DNA of our mitochondria, the organelles that create our energy supply on a molecular level. This impacts and impairs their ability to function correctly and creates a myriad of energy issues as we age. The most prevalent and dangerous types of mutations are the large deletions of DNA – which completely take over the cell and outcompete healthy mitochondria through a mechanism that hides them in plain sight. The Goal To prevent cells from being overrun by highly mutated mitochondria, the mechanism that cloaks them from detection and ..read more

New Human Trial Revelations Show Clearing Beta-Amyloid Early is Even More Effective Short summary: 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. In a previous blog post, we shared the thrilling news that clinical trials ha ..read more