Lifeboat Foundation

The skin is the largest organ of the body, comprising several compartments and about 20 different cell types that are involved in various skin functions – complexity that is more than skin deep! [1] Skin aging is a multifactorial process that is impacted by several intrinsic and extrinsic factors. Constant exposure of the human skin to such stimuli impacts its function and accelerates aging resulting in dry skin, wrinkling, thinning of the epidermis, and reduced barrier integrity. While we notice most of those changes by looking in a mirror – something the cosmetics industry has leveraged to multi-billion dollar effect – older skin is more at risk of injury, less able to sense touch, heat and cold, slower to heal and more prone to cellulitis and other skin infections.

Aging is a complex and gradual process characterized by a reduction in function and reproducibility along with an increase in the incidence of degenerative diseases. Skin aging has been reported to be associated with the presence and accumulation of senescent cells. “A number of diseases that increase in older people may have a unifying underlying mechanism having to do with senescence,” says Ruth Montgomery, PhD, professor of medicine and epidemiology (microbial diseases) at Yale School of Medicine [2].

Senescent cells are those that have lost their proliferative capacity, are resistant to apoptosis, and secrete factors that can cause tissue deterioration and inflammation [3]. These factors are termed senescence-associated secretory phenotype (SASP) and can lead to extracellular matrix (ECM) deposition, impact epidermal stem cell renewal and worsen melanin synthesis.

Heterochronic parabiosis ameliorates age-related diseases in mice, but how it affects epigenetic aging and long-term health was not known. Here, the authors show that in mice exposure to young circulation leads to reduced epigenetic aging, an effect that persists for several months after removing the youthful circulation.

Yang and co-workers state that “using inducible changes to the epigenome, we find that the act of faithful DNA repair advances aging at physiological, cognitive, and molecular levels, including erosion of the epigenetic landscape, cellular exdifferentiation, senescence, and advancement of the DNA methylation clock, which can be reversed by OSK-mediated rejuvenation. These data are consistent with the information theory of aging, which states that a loss of epigenetic information is a reversible cause of aging.” There is extensive evidence that the key reagent, restriction endonuclease I-PpoI, is cytotoxic. Moreover, the corresponding author published two papers—neither cited—showing that I-PpoI targeted to specific cell types causes a p53 response and cell elimination within a month. Despite globally inducing I-PpoI activation for seven times as long as required to induce a progeric effect, no analysis of mice during this critical window was presented. No significant conclusion of Yang was demonstrated.

In Switzerland, there’s a new cryonics company: and they invited me to have a look around. I had questions: legal, practical, and ethical, and I want to be clear: this is not an endorsement. I just wasn’t going to turn down that invitation. ■ Tomorrow Bio: https://www.tomorrow.bio/

Camera: Martin Bäbler.

Continue reading “Storing dead people at —196°C” »

As we age, our bodies undergo various changes that can impact our overall health and make us more susceptible to diseases. One common factor in the aging process is low-grade inflammation, which contributes to age-related decline and impairment. However, the precise pathways responsible for this inflammation and their impact on natural aging have remained elusive until now.

A new study led by Andrea Ablasser at EPFL now shows that a molecular signaling pathway called cGAS/STING plays a critical role in driving chronic inflammation and functional decline during aging. By blocking the STING protein, the researchers were able to suppress inflammatory responses in senescent cells and tissues, leading to improvements in tissue function.

The findings are published in the journal Nature.

A process of surgically joining the circulatory systems of a young and old mouse slows the aging process at the cellular level and lengthens the lifespan of the older animal by up to 10%.

Published in the journal Nature Aging, a study led by researchers at Duke University Medical Center in Durham, North Carolina, found that the longer the animals shared circulation, the longer the anti-aging benefits lasted once the two were no longer connected.

The findings suggest that the young benefit from a cocktail of components and chemicals in their blood that contributes to vitality, and these factors could potentially be isolated as therapies to speed healing, rejuvenate the body, and add years to an older individual’s life.

Year 2017 😗😁

The brain is really little more than a collection of electrical signals. If we can learn to catalogue those then, in theory, you could upload someone’s mind into a computer, allowing them to live forever as a digital form of consciousness, just like in the Johnny Depp film Transcendence.

Continue reading “Scientists Put a Worm Brain in a Lego Robot Body — And It Worked” »

Researchers have used 3D nanotechnology to successfully grow human retinal cells, opening the door to a new way of treating age-related macular degeneration, a leading cause of blindness in the developed world.

In age-related macular degeneration (AMD), the macula, the part of the retina that controls sharp, straight-ahead vision, deteriorates and causes blurring in the central field of vision.

There are two types of AMD, ‘dry’ and ‘wet.’ Dry AMD is where the RPE cells in the macula break down, causing vision loss over time. It’s the most common type and mostly affects older people. In the rarer wet AMD, abnormal blood vessel growth into the macula causes fluid and blood leakage, damaging the retina and destruction of the RPE cells, leading to a rapid loss of vision.

An expert on aging thinks humans could live to be 1,000 years old—with a few tweaks to our genetic “software”.