Lifeboat Foundation

Mind uploading and digital immortality explore the potential of AI technology to enable humans to live forever by transferring consciousness to machines. This concept raises profound questions about the future of humanity, identity, and ethics. Discover the groundbreaking possibilities and challenges of achieving eternal life through artificial intelligence and digital consciousness.

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This lifeform’s extraordinary biology could hold the key to anti-aging breakthroughs.

Researchers have discovered that DNA methylation is crucial for reprogramming astrocytes into stem cells in the adult mouse brain, especially after ischemic injury, with potential implications for regenerative medicine.

Some of our closest invertebrate cousins, like this Acorn worm, have the ability to perfectly regenerate any part of their body that’s cut off — including the head and nervous system. Humans have most of the same genes, so scientists are trying to work out whether human regeneration is possible, too.

Regeneration – now that’d be a nice superpower to have. Injure an arm? Chop it off and wait for it to grow back. Dicky knee? Ingrown toenail? Lop off your leg and get two for one!

It sounds ridiculous, but there’s a growing number of scientists that believe body part regeneration is not only possible, but achievable in humans. After all, not only are there plenty of animals that can do it, we can do it ourselves for our skin, nails, and bits of other organs.

COPENHAGEN, Denmark — In the never-ending quest to unlock the secrets of a long and healthy life, researchers at the University of Copenhagen have made a remarkable discovery. Their study has identified a specific gene that plays a crucial role in extending longevity across various species, including humans.

Publishing their work in the journal Cell Reports, researchers say the gene in question is called OSER1, and it encodes a protein that the team has dubbed a “novel pro-longevity factor.”

“We identified this protein that can extend longevity. It is a novel pro-longevity factor, and it is a protein that exists in various animals, such as fruit flies, nematodes, silkworms, and in humans,” says Professor Lene Juel Rasmussen, the senior author behind the study, in a media release.

Cellular senescence is a diverse phenotype characterised by permanent cell cycle arrest and an associated secretory phenotype (SASP) which includes inflammatory cytokines. Typically, senescent cells are removed by the immune system, but this process becomes dysregulated with age causing senescent cells to accumulate and induce chronic inflammatory signalling. Identifying senescent cells is challenging due to senescence phenotype heterogeneity, and senotherapy often requires a combinatorial approach. Here we systematically collected 119 transcriptomic datasets related to human fibroblasts, forming an online database describing the relevant variables for each study allowing users to filter for variables and genes of interest. Our own analysis of the database identified 28 genes significantly up-or downregulated across four senescence types (DNA damage induced senescence (DDIS), oncogene induced senescence (OIS), replicative senescence, and bystander induced senescence) compared to proliferating controls. We also found gene expression patterns of conventional senescence markers were highly specific and reliable for different senescence inducers, cell lines, and timepoints. Our comprehensive data supported several observations made in existing studies using single datasets, including stronger p53 signalling in DDIS compared to OIS. However, contrary to some early observations, both p16 and p21 mRNA levels rise quickly, depending on senescence type, and persist for at least 8–11 days. Additionally, little evidence was found to support an initial TGFβ-centric SASP. To support our transcriptomic analysis, we computationally modelled temporal protein changes of select core senescence proteins during DDIS and OIS, as well as perform knockdown interventions. We conclude that while universal biomarkers of senescence are difficult to identify, conventional senescence markers follow predictable profiles and construction of a framework for studying senescence could lead to more reproducible data and understanding of senescence heterogeneity.

Multiple studies now suggest that the accumulation of senescent cells is causal in ageing (Childs et al., 2015; Mylonas and O’Loghlen, 2022; van Deursen, 2014; Wlaschek et al., 2021), and their ablation extends healthspan and mean lifespan in rodents (Baker et al., 2016; Baker et al., 2011). Novel senolytic and senostatic drugs are in development (Kim and Kim, 2019; Niedernhofer and Robbins, 2018) with some drugs in clinical trials (Hickson et al., 2019; Justice et al., 2019) which might shortly lead to treatments capable of improving healthspan and extending lifespan in humans. However, the exact nature of senescent cells is often difficult to define, with multiple studies indicating that the most common biomarkers of senescence show different profiles across cell lines, types of senescence inducer, and the timepoint after the initial stimulus (Avelar et al., 2020; Basisty et al., 2020; Casella et al., 2019; Hernandez-Segura et al., 2017; Neri et al., 2021).

Aging is known to have profound effects on the human brain, prompting changes in the composition of cells and the expression of genes, while also altering aspects of the interaction between genes and environmental factors. While past neuroscience studies have pinpointed many of the molecular changes associated with aging, the age-related genetic factors influencing specific neuron populations remains poorly understood.

Recent studies on flies, mice, primates and human brain tissue utilizing single-cell or single-nucleus RNA-sequencing and genetic experimental techniques shed new light on these cell-type-specific changes. For instance, they unveiled the effects of aging on glial cells in the mouse and human brain, associations between cell-specific changes and modified chromatin proteins, and the influence of DNA methylation in the aging of various tissues.

Researchers at University of California (UC) San Diego and Salk Institute recently carried out a study aimed at better understanding how both age and sex impact human cortical neurons at a single-cell level. Their findings, published in Neuron, offer new insights into how aging affects cell composition, gene expression and DNA methylation across human brain cell types, while also uncovering differences between gene expression and DNA methylation in females and males.

Here the notorious but eloquent transhumanism critic Wesley J. Smith takes a swipe at the quickly growing movement to overcome death with science. New story in Merion West!

“Utopians often produce evil because their movement’s aspirations become paramount —that is, more important than avoiding acts ‘traditionally perceived as immoral.’ If enough people follow Istvan on the transhuman roller coaster, people could eventually get hurt.”

“I’m not afraid of dying. I just don’t want to be there when it happens.” – Woody Allen.

Continue reading “Why Transhumanism Is Unrealistic and Immoral” »

Researchers at The University of Texas MD Anderson Cancer Center have shown that therapeutically restoring ‘youthful’ levels of a specific subunit of the telomerase enzyme can significantly reduce the signs and symptoms of aging in preclinical models. If these findings are validated in clinical trials, they could have important therapeutic implications for age-related diseases such as Alzheimer’s, Parkinson’s, heart disease, and cancer.

The study, published in Cell, identified a small molecule compound that restores physiological levels of telomerase reverse transcriptase (TERT), which normally is repressed with the onset of aging. Maintenance of TERT levels in aged lab models reduced cellular senescence and tissue inflammation, spurred new neuron formation with improved memory, and enhanced neuromuscular function, which increased strength and coordination.

The researchers show that TERT functions not only to extend telomeres, but also acts as a transcription factor to affect the expression of many genes directing neurogenesis, learning and memory, cellular senescence, and inflammation.