Lifeboat Foundation

The whole interview is good and informative but starts with Sinclair commenting that at the moment he thinks living to 150 is possible in our lifetimes but not immortality. But given that, I’m 51. If I’m going to live potentially another century the technology will get better and better in that century and I would fully expect to life spans to become what we want rather than what we have to accept.

In this Ask Me Anything session, David and Peter discuss the latest age-reversal breakthroughs, getting approval from the FDA, and the possibility of living forever.
David Sinclair is a biologist and academic known for his expertise in aging and epigenetics. Sinclair is a genetics professor and the Co-Director of Harvard Medical School’s Paul F. Glenn Center for Biology of Aging Research. He’s been included in Time100 as one of the 100 Most Influential People in the World, and his research has been featured all over the media. Besides writing a New York Times Best Seller, David has co-founded several biotech companies, a science publication called Aging, and is an inventor of 35 patents.
Read David’s book, Lifespan: Why We Age-and Why We Don’t Have To: https://a.co/d/85H3Mll.

Continue reading “David Sinclair’s AMA: Age Reversal Breakthroughs, FDA Approval, and Living Forever” »

Leprosy is a chronic infectious disease caused by the bacterium Mycobacterium leprae. It affects the skin, nerves, and mucous membranes, and can lead to severe disfigurement and disability if left untreated.

Leprosy, a chronic infectious disease caused by the bacterium Mycobacterium leprae, is one of the oldest and most persistent diseases in the world. However, new surprising research suggests that the bacteria that cause leprosy may also have the ability to stimulate the growth and regeneration of the liver in adult animals without causing damage or scarring. Scientists have discovered that parasites associated with leprosy can reprogram cells to increase the size of the liver.

The findings suggest the potential to use this natural process to rejuvenate aging livers and extend the period of disease-free living in humans, known as healthspan. It may also be possible to use this process to regenerate damaged livers, potentially reducing the need for liver transplantation, which is currently the only effective treatment for individuals with severely scarred livers.

3D printers to create rapid on-demand objects have only been around for a short time. It’s a popular technique for making quick mock-ups or temporary solutions, but 3D-printing can also be used for more long-term applications. For example, some museums used it to create tactile models for interactive displays or even to create structural parts to support restoration projects. Either way, these are not temporary whimsical creations, but structures that they would likely still want to be in perfect shape several years down the line.

There are also other reasons to want to preserve 3D-printed materials for more than just a few years, but we haven’t had the technology for long enough to really know what will happen to these objects over time.

To find out, art conservation researchers at the Universidad Complutense de Madrid in Spain subjected two types of 3D printing materials to an artificial accelerated aging process. When plastics age, any damage such as loss of color or chemical changes in the materials are often caused either by UV radiation from exposure to light or by extreme temperature fluctuations. To simulate these extreme environments in a much faster scale than natural aging, the researchers put the 3D printed samples and the original filaments in two different chambers: One exposing the samples to UV light and the other subjecting them to a range of high temperatures.

At first, Professor Wolf Reik couldn’t quite believe the data. The experiment had involved an attempt to “rejuvenate” skin cells taken from a 53-year-old volunteer.

The results were better than anybody had expected: having been bathed in a cocktail of proteins, the cells now looked and behaved like those from somebody in their early twenties.

As different measurements of “biological age” confirmed the findings, the molecular biologist’s scepticism gave way to excitement. “I was falling off my chair three times over,” Reik said.

Anatomical decision-making by cellular collectives: Bioelectrical pattern memories, regeneration, and synthetic living organisms.

A key question for basic biology and regenerative medicine concerns the way in which evolution exploits physics toward adaptive form and function. While genomes specify the molecular hardware of cells, what algorithms enable cellular collectives to reliably build specific, complex, target morphologies? Our lab studies the way in which all cells, not just neurons, communicate as electrical networks that enable scaling of single-cell properties into collective intelligences that solve problems in anatomical feature space. By learning to read, interpret, and write bioelectrical information in vivo, we have identified some novel controls of growth and form that enable incredible plasticity and robustness in anatomical homeostasis. In this talk, I will describe the fundamental knowledge gaps with respect to anatomical plasticity and pattern control beyond emergence, and discuss our efforts to understand large-scale morphological control circuits. I will show examples in embryogenesis, regeneration, cancer, and synthetic living machines. I will also discuss the implications of this work for not only regenerative medicine, but also for fundamental understanding of the origin of bodyplans and the relationship between genomes and functional anatomy.

How do our bodies know what to become?

There are no instructions in our genes that code for the exact 3D structure of our bodies. There’s no tiny human contained in our DNA. So, what powers the transformation of the first cell in the embryo to a full-blown organism?

Continue reading “#14 Michael Levin — Our Body is a Collection of Intelligent Organisms” »

Scientists have found an extremely subtle twist in the genetics of aging cells, one that seems to make them increasingly less functional as time goes on.

R esearchers from Northwestern University have revealed animals like mice, rats, killifish, and even humans show a gradual imbalance of long and short genes in virtually every cell in their body as they age.

The discovery suggests there aren’t specific genes that control the aging process. Instead, old age seems to be governed by systems-level changes with complex effects. And this can impact thousands of different genes and their respective proteins.

Fluid intelligence refers to the ability to solve challenging novel problems when prior learning or accumulated experience are of limited use. ¹ Fluid intelligence ranks amongst the most important features of cognition, correlates with many cognitive abilities (e.g. memory), ² and predicts educational and professional success, ³ social mobility, ⁴ health ⁵ and longevity. ⁶ It is thought to be a key mental capacity involved in ‘active thinking’, ⁷ fluid intelligence declines dramatically in various types of dementia ⁸ and reflects the degree of executive impairment in older patients with frontal involvement. ⁹ Despite the importance of fluid intelligence in defining human behaviour, it remains contentious whether this is a single or a cluster of cognitive abilities and the nature of its relationship with the brain. ¹⁰

Fluid intelligence is traditionally measured with tests of novel problem-solving with non-verbal material that minimize dependence on prior knowledge. Such tests are known to have strong fluid intelligence correlations in large-scale factor analyses. ^{11, 12} Raven’s Advanced Progressive Matrices ¹³ (APM), a test widely adopted in clinical practice and research, ¹⁴ contains multiple choice visual analogy problems of increasing difficulty. Each problem presents an incomplete matrix of geometric figures with a multiple choice of options for the missing figure. Less commonly, verbal tests of fluid intelligence such as Part 1 of the Alice Heim 4 (AH4-1) ¹⁵ are adopted. The Wechsler Adult Intelligence Scale (WAIS) ¹⁶ has also been used to estimate fluid intelligence by averaging performance on a diverse range of subtests. However, several subtests (e.g. vocabulary) emphasize knowledge, disproportionately weighting measures of ‘crystallized’ intelligence, ^{17, 18} whilst others (e.g. picture completion) have rather low fluid intelligence correlations. ¹⁹ Hence, it has been argued that tests such as the APM are the most suitable for a theoretically-based investigation of changes in fluid intelligence after brain injury. ^{20, 21}

Proposals regarding the neural substrates of fluid intelligence have suggested close links with frontal and parietal functions. For example, Duncan and colleagues ²² have argued that a network of mainly frontal and parietal areas, termed the ‘multiple-demand network’ (MD), is ‘the seat’ of fluid intelligence. The highly influential parieto-frontal integration theory (P-FIT), based largely on neuroimaging studies of healthy subjects, posits that structural symbolism and abstraction emerge from sensory inputs to parietal cortex, with hypothesis generation and problem solving arising from interactions with frontal cortex. Once the best solution is identified, the anterior cingulate is engaged in response selection and inhibition of alternatives. ^{23, 24} Despite its name, P-FIT also posits occipital and temporal involvement, implying widely distributed substrates of fluid intelligence.

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Want to donate with cryptocurrency? Lifespan.io is proud to announce the official launch of the Longevity Cause Fund in partnership with Sens Research Foundation and the Methuselah Foundation, facilitated by Angel Protocol.

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