Oldest known animal killed and secrets of immortality.
Ming the ocean quahog lived peacefully for over 500 years off the coast of Iceland. So why did a team of researchers dredge it up and kill it?
Category: life extension – Page 129
Discover the fascinating world of digital immortality and the pivotal role artificial intelligence plays in bringing this concept to life. In this captivating video, we delve into the intriguing idea of preserving our consciousness, memories, and personalities in a digital realm, potentially allowing us to live forever in a virtual environment. Unravel the cutting-edge AI technologies like mind uploading, AI-powered avatars, and advanced brain-computer interfaces that are pushing the boundaries of what it means to be alive.
Join us as we explore the ethical considerations, current progress, and future prospects of digital immortality. Learn about the ongoing advancements in brain-computer interfaces such as Neuralink, AI-powered virtual assistants like ChatGPT, and the challenges and opportunities that lie ahead. Will digital immortality redefine humanity’s relationship with life, death, and existence itself? Watch now to uncover the possibilities.
Keywords: digital immortality, artificial intelligence, mind uploading, AI-powered avatars, brain-computer interfaces, Neuralink, ChatGPT, virtual afterlife, eternal life, neuroscience, ethics, virtual reality, consciousness, future of humanity.
New research by biotech Integrated Biosciences and scientists from MIT and the Broad Institute of MIT and Harvard has demonstrated the potential of AI in discovering novel senolytic compounds.
Longevity. Technology: Senolytics are small molecules that suppress age-related processes such as fibrosis, inflammation and cancer. They target senescent cells – the so-called ‘zombie’ cells that are no longer dividing, emit toxic chemicals and are a hallmark of aging. Senescent cells have been linked to various age-related diseases, including cancer, cardiovascular disease, diabetes and Alzheimer’s disease, but senolytic compounds can tackle them by selectively inducing apoptosis or programmed cell death in these zombie cells. This new research reduced the number of senescent cells and lowered the expression of senescence-associated genes in aged mice, results which, the authors say “underscore the promise of leveraging deep learning to discover senotherapeutics” [1].
The AI-guided screening of more than 800,000 compounds led to the identification of three drug candidates, which, when compared with senolytics currently under investigation, were found to have comparable efficacy and superior medicinal chemistry properties [1].
Human lifespan is intricately connected to the aging process of individual cells, and this means that scientists have spent decades trying to unravel the mysteries of cellular aging and exploring methods to slow down the ticking of the aging clock.
Longevity. Technology: In 2020, a group of researchers from the University of California San Diego identified two distinct mechanisms of cellular aging and genetically manipulated them to extend cell lifespan [1]. Now, their research has progressed to employ synthetic biology and gene circuits to delay the deterioration associated with cellular aging [2]. The team’s innovative approach could revolutionize scientific methods of aging prevention and contribute to reprogramming aging pathways in various human cell types.
Publishing in Science, the researchers describe how cells in yeast, plants, animals and humans all contain gene regulatory circuits responsible for several physiological functions, including aging. These gene circuits, akin to electric circuits controlling household devices, can operate in different ways, and the UC San Diego team discovered that cells don’t necessarily age the same way – it all depends on their genetic material and environment. The researchers found that cells can age either through DNA stability decline or mitochondrial decline.
Biologist David Sinclair takes 7 supplements and 2 prescription medications to boost longevity. Here’s his full supplement stack.
In a study of 17 people from five families, Johns Hopkins Medicine researchers say they found that ultra-lengthy DNA endcaps called telomeres fail to provide the longevity presumed for such people. Instead, people with long telomeres tend to develop a range of benign and cancerous tumors, as well as the age-related blood condition clonal hematopoiesis.
Reporting in the May 4 issue of the New England Journal of Medicine, the Johns Hopkins researchers say clonal hematopoiesis is common among this long-telomere group, and the blood condition combined with long telomeres may help mutations stick around longer in blood cells.
“Our findings challenge the idea that long telomeres protect against aging,” says Mary Armanios, M.D., professor of oncology at the Johns Hopkins Kimmel Cancer Center, and professor of genetic medicine, molecular biology and genetics, and pathology at the Johns Hopkins University School of Medicine. “Rather than long telomeres protecting against aging, long telomeres allowed cells with mutations that arise with aging to be more durable.”
Drug company Eli Lilly reports that donanemab can slow the pace of Alzheimer’s disease by 35%, following a Phase 3 study in human patients.
Brain scans of Alzheimer’s patients with treatment (A and B) and placebo ©, showing clearance of amyloid plaques. Credit: Eli Lilly.
In recent years, Alzheimer’s has become an increasingly major public health issue. The prevalence of this disease – a progressive neurological disorder that affects memory, thinking, and behaviour – is being driven by aging populations, changes in lifestyle factors, and improvements in diagnostic techniques.
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For Rance and others in the field, fezolinetant’s progress to this point is a sign that research into the causes and effects of menopausal symptoms is finally being taken seriously. In the next few years, the global number of postmenopausal women is expected to surpass one billion. But many women still struggle to access care related to menopause, and research into how best to manage such symptoms has lagged behind. That is slowly changing. Armed with improved animal models and a growing literature on the effects of existing treatments, more researchers are coming into the field to fill that gap.
They increasingly recognize that menopause and the transition to it, a phase labelled perimenopause, could set the stage for brain health in later life, and there are even hints that it could correlate with the risk of neurodegenerative diseases, such as Alzheimer’s disease.
Fezolinetant and similar drugs in the pipeline also represent a shift in thinking: from menopause as a condition of the female reproductive organs, to one that focuses on neurological causes and effects. “We think of menopause as being driven by changes in the ovary,” says Hadine Joffe, who studies mental health and ageing in women at Harvard Medical School in Boston, Massachusetts. “The notion of the brain at the helm of menopause, that is a different concept.”
Next week will see the first Sheba Longevity Conference, a meeting that will bring together all relevant stakeholders in the multidisciplinary field of longevity medicine, providing a forum for showcasing outstanding research and scientific breakthroughs. The conference will also include the opening ceremony of the public academic hospital longevity center at Sheba Hospital.
The conference aims to foster collaborations that will accelerate the translation of scientific discoveries into clinical practices and facilitate a shift in Israel’s national healthy longevity policy. The event will also include an exhibition space for sponsors, partners and industry representatives to promote dialogue and showcase their work.
Longevity. Technology: Kirkland, Rando, Barzilai, Maier, Zhavoronkov, Verdin, Mannick… the Sheba Longevity Conference has bagged some longevity A-listers who will be discussing senescence, geroscience, global longevity, aging clocks and more. We sat down with one of the founders of Sheba Longevity, Dr Evelyne Bischof, to find out more.