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Category: life extension – Page 6

Nectandrin B (Found In Nutmeg) Extends Lifespan As Much As Rapamycin

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Beyond BMI: Analysis links fat distribution to distinct brain aging patterns

Research led by The Hong Kong Polytechnic University finds that regional fat distribution exerts distinct effects on brain structure, connectivity and cognition, revealing patterns not explained by body mass index (BMI).

Obesity has been associated with structural and functional changes in the brain, including reductions in , disruptions in white matter and impaired connectivity, which have been associated with cognitive decline.

Previous studies frequently used BMI as the central measure of obesity, a highly generalized metric that cannot capture the biological differences in fat depots. Adipose tissue in different body regions is known to affect metabolic and inflammatory pathways differently, and earlier work has suggested that visceral (around organs in the ) and leg fat contribute unequally to disease risk.

Bilu Huang — CSO, Fuzhuang Therapeutics — Conquering Aging Via TRCS

Conquering aging via TRCS — the telomere DNA AND ribosomal DNA co-regulation model for cell senescence — bilu huang — CSO, fuzhuang therapeutics.

Bilu Huang (https://biluhuang.com/) is a visionary scientist dedicated to finding solutions to some of the most pressing challenges facing humanity. His interdisciplinary work spans multiple fields, including biological aging, dinosaur extinction theories, geoengineering for carbon removal, and controlled nuclear fusion technology.

Born in Sanming City, Fujian Province, Huang is an independent researcher whose knowledge is entirely self-taught. Driven by curiosity and a relentless pursuit of scientific exploration, he has achieved numerous research results through his dedication and passion for science.

As a talented theoretical gerontologist, he proposed the Telomere DNA and ribosomal DNA co-regulation model for cell senescence (TRCS) and he is now using this latest theory to develop biotechnology to rejuvenate cells which will be used to completely cure various age-related degenerative diseases and greatly extend human life at Fuzhuang Therapeutics (https://lab.fuzhuangtx.com/en/).

#Aging #Longevity #BiluHuang #FuzhuangTherapeutics #TelomereDNAAndRibosomalDNACoRegulationModelForCell #Senescence #TRCS #DinosaurExtinctionResearch #CarbonRemovalTechnology #ControlledNuclearFusion #TelomereDNA #RibosomalDNA #CellularAging #GeneticProgram #Telomere #P53

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How a key enzyme shapes nucleus formation in cell division

Every time a eukaryotic cell divides, it faces a monumental challenge: It must carefully duplicate and divide its genetic material (chromosomes) equally, and then rebuild the nuclear envelope around the separated halves. If this process goes wrong, the resulting nuclei can be misshapen or disorganized—features often seen in cancer and aging-related diseases.

A new study from researchers at the Indian Institute of Science (IISc) and Université Paris-Saclay reveals how a key enzyme called Aurora A helps cells pull off this feat. The findings are published in The EMBO Journal.

In dividing cells, structures called spindle poles (or centrosomes) grow in size to generate the microtubule ‘tracks’ that pull chromosomes apart. Once this job is done, the spindle poles must shrink and disassemble so that the can reform around the separated chromosomes.

The Muscle-Brain Axis and Neurodegenerative Diseases: The Key Role of Mitochondria in Exercise-Induced Neuroprotection

Regular exercise is associated with pronounced health benefits. The molecular processes involved in physiological adaptations to exercise are best understood in skeletal muscle. Enhanced mitochondrial functions in muscle are central to exercise-induced adaptations. However, regular exercise also benefits the brain and is a major protective factor against neurodegenerative diseases, such as the most common age-related form of dementia, Alzheimer’s disease, or the most common neurodegenerative motor disorder, Parkinson’s disease. While there is evidence that exercise induces signalling from skeletal muscle to the brain, the mechanistic understanding of the crosstalk along the muscle–brain axis is incompletely understood. Mitochondria in both organs, however, seem to be central players.

Rapamycin linked to DNA damage resilience in aging human immune cells

University of Oxford-led research finds low-dose rapamycin functions as a genomic protector in aging human immune cells, lowering DNA damage.

The mechanistic target of rapamycin (mTOR) is a central signaling pathway that regulates and coordinates cell growth, metabolism, and survival in response to environmental cues. It helps cells integrate signals from growth factors, nutrients, and stress to control whether they are in an anabolic (building up) or catabolic (breaking down) state.

Aging immune systems accumulate DNA damage linked to immunosenescence. Rapamycin is a drug that inhibits the mTOR pathway. Originally developed for organ transplantation to prevent immune rejection, previous research has found that, at non-immunosuppressive doses, rapamycin can mitigate cellular senescence.

Space Habitat Clusters & Conglomerations

Space isn’t just for lonely colonies—it’s for communities. Join us as we imagine constellations of space habitats bound by tethers, trade, and trust, building not just homes in the stars but entire civilizations.

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Chapters.
0:00 Intro.
1:13 Why Clustered Habitats?
6:00 Habitat Types and Roles Within Clusters.
9:41 Mobility and Modularity – The Politics of Moveable Worlds.
14:02 Tethers, Transit, and Shared Infrastructure.
17:35 Shapes of Clusters and Dynamic Conglomerations.
23:43 Nebula.
25:21 Digital Ecosystems and Cultural Identity.
25:19 Economics and Trade in Habitat Constellations.
26:52 Education and Intergenerational Planning.
28:17 Security and Conflict Management.
29:10 A Tale of Unity.
32:29 Religion, Ritual, and Meaning.
33:19 The Long View: Legacy and Civilization.
34:07 Closing Reflections

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Hi everybody. I’m writing to you because we are reaching an important moment in our reproduction of Harold Katcher’s seminal study of rats rejuvenation, in which we are only 9 months from starting the injections but we raised 71% of the total cost of the experiment. We already published the article of our 2024 experiment in a peer-reviewed journal (https://journals.tmkarpinski.com/index.php/ejbr/article/view/772), in which we injected the Pig Plasma Extracellular Particles (PPEPs) in young rats to assess a potential acute immunogenicity or toxicity — without any negative effect observed. Nina Torres Zanvettor (cofounder of ICR together with me) and I were interviewed some weeks ago by Eleanor Sheekey in her YouTube channel (https://youtu.be/Q-lS1UMHG1o?si=ImDWycjM8r8-KpyF), as we are trying to spread the word about the experiment and the crowdfunding. We are making the experiment in collaboration with Unicamp university and Dr. Marcelo Mori, a world-class aging scientist. The rats are already aging in the university facility and we are preparing the epigenetic age measurements with Horvath’s foundation (Clock Foundation), but we still have to raise 29% (US$21,000) of the total cost (US$75,000).

(https://youtu.be/Q-lS1UMHG1o

We will publish everything (methods, materials and results) immediately, but we need the help of the community too, as we will give back all the information for the community. Could you help us to fund the study? Any amount is important. The link to make a donation is https://www.rejuvenescimento.org/donation. I don’t even consider it precisely a “donation”, but a financial collaboration, as the “donor” would be able to use the information, and maybe they can also use the rejuvenation technology that some day would arise from this research. By the way, if we manage to rejuvenate the rats, we will then try to keep them young as long as we can, in a longevity experiment. Also, if we rejuvenate the rats, we will carry out a safety experiment in a Good Laboratory Practices facility here in Brazil that would allow regulatory approval to try the therapy in human patients who don’t have any other alternative to be kept alive — we expect to be able to carry out those human trials in 2028. So we intend to go all the way to the clinic, if we confirm Katcher’s results.

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