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).

Dec. 14, 2021 — A new FDA-approved eyedrop medicine could replace reading glasses for millions of Americans who have age-related blurry vision.

The product, called Vuity, was approved by the FDA in October and went on the market last week. The new medicine begins working in about 15 minutes and provides sharper vision for 6 to 10 hours.

Vuity is the first FDA-approved eyedrop to treat the condition known as presbyopia, which tends to affect people ages 40 and older. The prescription drug uses the eye’s natural ability to reduce its pupil size.

Researchers at UC San Francisco (UCSF) have engineered molecules that act like “cellular glue,” allowing them to direct in precise fashion how cells bond with each other. This discovery represents a major step toward building tissues and organs, a long-sought goal of regenerative medicine [1].

Longevity. Technology: Adhesive molecules are found naturally throughout the body, holding its tens of trillions of cells together in highly-organised patterns. They form structures, create neuronal circuits and guide immune cells to their targets. Adhesion also facilitates communication between cells to keep the body functioning as a self-regulating whole.

Now a new study, published in Nature, details how the researchers engineered cells containing customised adhesion molecules that bound with specific partner cells in predictable ways to form complex multicellular ensembles.

Awareness about aging and early symptom of disease can extend life to much more year.

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There has been plenty going on here at Lifespan.io, so we thought it was time to give you a little update on what’s been happening.

The Longevity Summit 2022 is happening on December 6–7 at the Buck Institute for Research on Aging, and Lifespan.io is an official media partner! As a special bonus to our readers, you can purchase tickets here with a 15% discount using the code LifespanIO.

Our Executive Director Stephanie Dainow will be hosting a discussion panel during the event. If you are at the conference, please do come and say hello, as we are always interested in meeting people in the industry and exploring ways to collaborate.