Lifeboat Foundation

The newly-created Longevity Escape Velocity Foundation (LEV) has released details of the first study in its flagship research programme: Robust Mouse Rejuvenation – Study 1.

Longevity. Technology: A highlight of Longevity Summit Dublin 2022 was Dr Aubrey de Grey’s announcement of his new foundation; LEV Foundation exists to proactively identify and address the most challenging obstacles on the path to the widespread availability of genuinely effective treatments to prevent and reverse human age-related disease, and to that end, its flagship research programme is a sequence of large mouse lifespan studies.

Mouse models are significant in aging research for several reasons. Mice and humans share many genetic and physiological similarities, including similar aging-related pathways, and this makes mice a useful model for studying the molecular and cellular processes underlying aging in humans.

Muscle injury induces cell senescence, which promotes inflammation.

We never stopped evolving.

Are humans still evolving? This question is a mystery for many, as about seven million years have passed since humans left the chimpanzee lineage. The factors that forced us to adapt, evolve, and survive harsh environments in the past are no longer relevant.

Continue reading “155 Newly Identified Genes Reveal Humans Are Continuously Evolving” »

We celebrate the Remembrance of the Resurrectables each year. A ceremony for remembering all of the patients that are in Cryonic Suspension awaiting an eventual return to a full healthy life.

Go To https://youtu.be/NgdwYAWCy88 for part 1 of our service: Dr. Richard Olree “Minerals for Telomeres” and “Age Reversal Update” with Bill Faloon.

Continue reading “COPL Remembrance of The Resurrectables 2022” »

But even junk has hidden treasures. Studies found variations in these unsequenced regions were intricately involved in human health, from aging to conditions like cancer and developmental disorders like autism. In 2022, a landmark study finally resolved the genomic unknown, completely sequencing the remaining eight percent of undeciphered DNA remaining.

Now, scientists are discovering that some genetic sequences encode proteins that lack any obvious ancestors, what geneticists call orphan genes. Some of these orphan genes, the researchers surmise, arose spontaneously as we evolved, unlike others that we inherited from our primate ancestors. In a paper published Tuesday in the journal Cell Reports, researchers in Ireland and Greece found around 155 of these smaller versions of DNA sequences called open reading frames (or ORF) make microproteins potentially important to a healthy cell’s growth or connected to an assortment of ailments like muscular dystrophy and retinitis pigmentosa, a rare genetic disease affecting the eyes.

“This is, I think, the first study looking at the specific evolutionary origins of these small ORFs and their microproteins,” Nikolaos Vakirlis, a scientist at the Biomedical Sciences Research Center “Alexander Fleming” in Greece and first author of the paper, tells Inverse. It’s an origin, he says, that’s been mired in much question and mystery.

Bened Biomedical scientists increase muscle strength and size and stimulate the ghrelin hormone with Lactobacillus parcasei PS23, a probiotic, in age-accelerated mice.

Throughout our lives, our skin goes through a lot. We get sunburns, we skin our knees, we bleed, we scar and we do it again. Our skin is our largest organ and, in many ways, serves as our protector. Beyond acting as a protective barrier between us and our environment, our skin regulates our body temperature, provides immune protection against harmful microbes and blocks out harmful sunlight in ways that benefit the whole body. And when skin is injured, blood brings healing substances to the site to promote healing as the body awaits new, replacement skin cells.

Regardless of scrapes and scratches, skin cells are constantly renewing themselves throughout our lives — a process reliant on skin stem cells. These skin stem cells turn over slowly, keeping our skin healthy and young. But as we age, these skin stem cells either numerically or functionally deplete, our skin thins and we are consequentially at higher risk for developing ulcers. The older the skin, the harder it is to heal these ulcers, meaning they can become chronic, open wounds that impact lifestyle and invite infection.

But what if we could activate a skin stem cell to be more responsive to injury? To get an 80-year-old’s skin to function like a 30-year-old’s skin? Could we reverse skin stem cell age-related deterioration and improve their turnover? What if we could do so in a way that healed wounds regeneratively, without any scarring? With these questions in mind, a collaborative team of researchers from the Mass General Brigham, Boston Children’s Hospital, and four additional Harvard institutions set off to study these powerful cells.

Partial somatic cell reprogramming has been touted as a promising rejuvenation strategy. However, its association with mechanisms of aging and longevity at the molecular level remains unclear. We identified a robust transcriptomic signature of reprogramming in mouse and human cells that revealed co-regulation of genes associated with reprogramming and response to lifespan-extending interventions, including those related to DNA repair and inflammation. We found that age-related gene expression changes were reversed during reprogramming, as confirmed by transcriptomic aging clocks. The longevity and rejuvenation effects induced by reprogramming in the transcriptome were mainly independent of pluripotency gain. Decoupling of these processes allowed predicting interventions mimicking reprogramming-induced rejuvenation (RIR) without affecting somatic cell identity, including an anti-inflammatory compound osthol, ATG5 overexpression, and C6ORF223 knockout. Overall, we revealed specific molecular mechanisms associated with RIR at the gene expression level and developed tools for discovering interventions that support the rejuvenation effect of reprogramming without posing the risk of neoplasia.

Aging is associated with the buildup of molecular damage and a gradual loss of function, culminating in chronic age-related diseases and ultimately death (1). Searching for safe and efficient interventions that can slow down or partially reverse the aging process is a major challenge in the aging field (2 – 6). In this regard, reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) has been proposed as a candidate longevity intervention due to its potential to rejuvenate cells in a targeted way (7, 8).

Pluripotency can be achieved in vitro by the ectopic expression of four transcription factors: OCT4, SOX2, KLF4, and MYC, known as OSKM or Yamanaka factors (YFs). It was demonstrated that OSKM support the generation of murine iPSCs using retroviral transduction as a delivery system and mouse embryonic fibroblasts (MEF) as the initial cell culture. Although this original experiment was inefficient in terms of the percentage of cells that terminally achieved the pluripotent state (0.1%), more advanced in vitro approaches resulted in a greatly improved efficiency, e.g. by down-regulation of methyl CpG-binding domain 3 (MBD3) levels (10). In parallel, other approaches have been developed to induce pluripotency. In particular, the expression of seven other transcription factors (7F: Jdp2-Jhdm1b-Mkk6-Glis1-Nanog-Essrb-Sall4) resulted in high efficiency of reprogramming (11).