Longevity InTime: Autonomous AI Institute. Anti-Aging Digital Health Immortality Transhumanist AI Channel

Steven Pinker compared Anthropic’s in‑house AI ethicists to the bioethicists of the Human Genome Project, saying he views both groups with the same suspicion. He wrote on X on 27 September that they argue in a vacuum, ignoring real‑world consequences, and linked his view to an investigation by Free Beacon about the philosophers Anthropic employs for its chatbot Claude, including Joe Carlsmith, who co‑authored the “Claude Constitution.” Anthropic has run a model‑welfare program for more than a year, trying to decide whether its AI systems deserve moral consideration, and the company itself admits there is no consensus on whether the models are conscious. Chris Anderson turned the idea into a testable case, noting that the Human Genome Project’s ethics program received a fixed 5% of the budget for years. Its conferences debated hypothetical insurance‑rate spikes from genetic risk—a threat that never materialised—while nobody foresaw that services like 23andMe would let people find distant relatives by DNA, even helping to catch criminals. In 2024, Undark and STAT News found that about 75% of the reference genome came from a 🔗 Read original →

Hippocampal reprogramming reverses Alzheimer's pathology and restores bone in mice Chinese researchers injected OSK (Oct4, Sox2, Klf4) via virus into the hippocampus of Alzheimer's model mice, omitting the oncogenic c‑Myc factor. Treatment reduced amyloid plaque buildup, calmed brain inflammation, and improved learning and memory at both early and advanced disease stages. Treated mice also showed recovery of spongy bone tissue in the femur, which had been thinned by disease, via particles released into blood after therapy. The study appeared Journal of Neuroinflammation on 28 May; results were highlighted by David Sinclair in a tweet on 27 September. The OSK factors (three of the four Yamanaka factors) partially rejuvenate cells without causing tumorigenic conversion; prior safety checks confirmed no stem‑cell markers appeared in microglia or neuron cultures. OSK lowered amyloid‑producing BACE1 activity, shifted microglia to a resting state, and preserved neurons, synapses, and myelin without organ damage or tumors after two months. DNA methylation sequencing showed disease‑associated methylation changes in neuronal circuit genes were erased, an effect dependent on the Tet2 demethylase. Previously, the same lab found Alzheimer’s brains release extracellular vesicles that push bone‑marrow stem cells toward fat instead of bone; after hippocampal reprogramming, vesicle miR‑483‑5p dropped, allowing bone formation to resume even though only the brain was treated. Blocking miR‑483‑5p alone reproduced the bone‑rescue effect, confirming a brain‑to‑bone signaling pathway. Earlier work by Johannes Gräff’s lab at EPFL reprogrammed only memory‑related neurons in old mice; here whole‑hippocampus delivery yielded broader benefits, including stronger amyloid reduction and systemic bone improvement. 🔗 Read original →

Stanford Experts Warn Consumer Biological Age Tests Are a 'Wild West' Tony Wyss‑Coray, a co‑creator of modern aging clocks at Stanford, calls the consumer biological‑age‑test market a “Wild West.” On September 25 Stanford Medicine published an analysis in which neuroscientist Tony Wyss‑Coray, geneticist Anne Brunet, and epidemiologist David Rehkopf explained what different biological‑age tests measure and why their results diverge. Rehkopf estimates that many epigenetic tests have a built‑in error of about three years, while one of the most thoroughly vetted anti‑aging drugs shows the opposite shift on those clocks. In humans taking studied doses of rapamycin, the epigenetic clocks instead indicate slight aging. A similar mismatch appeared in the RAPA‑EX‑01 trial, where rapamycin plus home exercise did not boost strength in older adults and four epigenetic clocks there showed no expected rejuvenation. Chronological age is simply the number of years lived; biological age estimates how fast the body is wearing down and how many healthy years remain. Commercial tests sell that number for a few hundred dollars, using a drop of blood, saliva, or fitness 🔗 Read original →

Genetic program, not damage, drives aging, says biologist Petr Lidsky On 27 September aging biologist Petr Lidsky posted on X that no other disease is considered to be caused by damage, so aging should not be an exception. He was challenged by evolutionary biologist Alexander Wolf, who cited cancer, and by Mike Lee, who pointed to a 2025 study of an enzyme that re 🔗 Read original →

Peter Thiel: Christianity Beats Transhumanism with Eternal Body, Transformed Soul On September 24 in Berlin, Peter Thiel received the Axel Springer Award and spoke for over an hour with CEO Mathias Döpfner. Near the end, Döpfner asked about the most optimistic scenario for human lifespan. Thiel cited a target of 150 years, saying there is no clear natural limit, rejected mind‑uploading as a route to immortality, and said he would prioritize work on dementia. Döpfner, head of Axel Springer (which owns Bild, Die Welt, Politico and Business Insider), then asked Thiel to name the boldest scenario and himself suggested “eternal life.” Thiel replied, “**150 years 🔗 Read original →

Pop‑Corn Method Improves Prediction of Cell‑Type Changes After Gene Knockouts On September 26, researchers from Yale University and the Whitehead Institute for Biomedical Research released a preprint describing the new Pop‑Corn method for predicting how gene knockouts reshape cellular populations. It was tested on both cultured cells and living tissue. In a benchmark of almost 58 000 human T‑cells, Pop‑Corn reproduced the post‑perturbation cell‑type composition more accurately than four existing models (GEARS, scGPT, CPA, CellFlow) and better preserved rare states. Its composition‑reconstruction correlation reached 0.802, compared with 0.187 for CPA, 0.629 for scGPT, 0.681 for CellFlow and 0.709 for GEARS. To gauge usefulness, the team ranked genes by predicted effect on cell state and compared the top‑5 predictions with experimental results, finding 🔗 Read original →

APOE4‑driven brain‑vessel scarring linked to Alzheimer’s reversed in mice and human brain model Researchers from the Icahn School of Medicine at Mount Sinai reported in Cell, September 24, 2024 that the APOE4 gene triggers scarring of brain blood vessels, a process that leads to Alzheimer’s disease, and that this scarring can be reversed in mice and a laboratory model of human brain tissue (miBrain). Carriers of APOE4 have especially fragile brain vessels that accumulate toxic amyloid. In APOE4 carriers, vascular support cells known as pericytes transform into scar‑forming myofibroblast‑like cells that attract amyloid to the vessels; this transition is reversible. Normally, pericytes wrap the brain’s smallest vessels and help maintain the blood‑brain barrier. An atlas of gene activity in roughly 64 000 vascular cells from 220 people showed 🔗 Read original →

Metformin Anti‑Aging Trial TAME Stalled Despite FDA Approval The TAME trial, designed by Nir Barzilai and colleagues at Albert Einstein College of Medicine, aims to enroll over 3,000 participants aged 65–79 at 14 U.S. sites to test whether metformin can delay a cluster of age‑related diseases — heart attack, cancer, dementia, and death — by treating aging itself as a composite endpoint. It received FDA protocol approval in 2015 for this novel outcome measure. Despite the regulatory green light, the trial has not enrolled a single patient after more than ten years because it 🔗 Read original →

Philosopher David Pearce Calls for Gene Editing Inspired by Pain‑Insensitive Scotswoman In an interview released on 30 August on the YouTube channel New Horizons, philosopher David Pearce – co‑founder of the World Transhumanist Association in 1998 with Nick Bostrom – argued that future parents should edit the genomes of their children to emulate the pain‑insensitive trait of Scottish woman Jo Cameron. He presented her case as a model to copy, not as an innate inability to feel pain. Jo Cameron carries a double mutation in the FAAH-OUT gene that reduces FAAH enzyme activity, leaving her with twice the normal level of anandamide, the ‘bliss’ molecule. As a result, her pain threshold is unusually high – surgeries and childbirth felt like a tickle – while wound healing is faster and anxiety is reduced. Pearce proposes that parents use pre‑implantation screening and genome editing to raise everyone’s pain threshold and hedonic set‑point to Cameron’s level. For wild species he advocates CRISPR gene drives to spread the edit rapidly, replacing hunger and predation with population management, up 🔗 Read original →

AI in biology limited by lack of real‑time cell‑reading tools, says Harvard biologist Alex Plesa, a biologist at Harvard, argues that the slowdown in AI‑driven biology stems not from insufficient data but from the absence of instruments capable of reading and altering a living cell’s state in real time. He made this point in a Substack essay titled “AI for biology does not need additional data,” published 15 September. Current approaches to studying a cell destroy it and measure the activity of 20,000 genes only once, whereas a living cell such as a neutrophil senses, decides, and acts continuously, like a neutrophil chasing a bacterium. Over ten years of building cell‑aging models, Plesa had only averaged measurements across hundreds of cells, lacking the time‑resolved data needed to control an individual cell rather than a mean of millions of dead cells. Any molecular‑biology method sacrifices one of three attributes: speed, non‑destructiveness, or breadth. Microscopy tracks merely 3–4 proteins; RNA‑sequencing yields thousands of readouts but kills the cell and takes days. No technique provides all three 🔗 Read original →

Kevin Esvelt Warns AI Could Enable Easy Reconstruction of 1918 Flu Virus On September 13, physicist Sam Rodriguez of FutureHouse and David Bellami dismissed AI bioweapon fears as panic. Three days later, on September 16, Kevin Esvelt replied that such silence costs lives, noting Rodriguez’s claim that evolution quickly removes harmful mutations and Bellami’s label of the fears as “complete nonsense.” Esvelt’s first proof showed that 36 of 38 DNA‑synthesis companies sent fragments of the 1918 flu virus and the ricin gene when ordered by a student without a lab; the fragments allowed several full reconstructions, and synthetic DNA for the virus cost about $3000. Screening missed pieces shorter than 50 base pairs, though SecureDNA catches them but is not mandatory; only one company requested identity verification (due to ricin) and overlooked the flu fragments. His second proof came from a language model that revealed a novel bioweapon to Esvelt that he had not imagined, requiring only deeper knowledge of narrow biology fields rather than special creativity; the model out‑prepared a top expert, weakening the argument “AI isn’t as strong as experts.” Esvelt agrees that evolution strips transmission‑hindering mutations, but for a single outbreak the virus need not be stable forever; a model that pre‑selects immune‑evading mutations could make vaccines insufficient protection. His lab is building SecureBio to screen wastewater and swabs for unknown pathogens as a backup if DNA screening fails. He proposes opening OpenAI’s GPT‑Rosalind model to researchers with verifiable publications, while refusing to train downloadable open models on molecular‑biology data; without such access China would have to build a parallel closed model. He does not believe superintelligent AI will instantly master atomic design because bio‑design models are limited by lack of experimental gene‑function data, not size. The debate over future AI speed continues despite the proven screening failure: 36 of 38 suppliers let the flu fragments through, and the virus that once killed 50 million people could be recreated for a few thousand dollars. 🔗 Read original →

Scientists target rare aging macrophages that shield liver and lung tumors with fibrosis Researchers at Memorial Sloan‑Kettering Cancer Center, led by Scott Lowe, identified a rare subset of aged macrophages that express the surface protein P‑selectin and drive fibrosis around liver and lung tumors. These cells create a collagen‑rich barrier that keeps immune cells out and dampens any that infiltrate, rendering immunotherapy largely ineffective. The work was published Science, September 24. To reach these macrophages, the team packaged the previously failed drugs Navitoclax and dBET6 into nanoparticles made from fucoidan, a polysaccharide that binds P‑selectin. The fucoidan‑based particles deliver the drugs specifically to the P‑selectin‑positive macrophages, sparing other cells. In mouse models, the nanoparticles cleared liver and lung fibrosis as well as free drugs but did not cause the thrombocytopenia seen with systemic Navitoclax or dBET6 treatment. Tumors growing in fibrotic organs became sensitive to immunotherapy, showing regression when the nanoparticles were combined with checkpoint blockade; the effect depended on CD8⁺ T‑cells. The pathogenic macrophages constitute only 3–5% of the fibrotic tissue, yet their removal markedly reduces fibrosis. Earlier genetic ablation of senescent macrophages using the intracellular marker p16 showed a similar benefit, but p16 is not surface‑exposed, limiting drug targeting. P‑selectin provides the needed extracellular marker for precise nanoparticle delivery. Analysis of human lung and liver tumor samples confirmed the presence of the same P‑selectin‑positive macrophage subset, with higher numbers correlating to greater fibrosis and poorer response to immunotherapy. Nanoparticles killed this subset in patient‑derived samples without affecting surrounding cells. Reviving Navitoclax and dBET6 through this selective delivery strategy could rescue the drugs for clinical use, and MSK is seeking partners to test the approach. 🔗 Read original →

Liver‑specific growth hormone receptor knockout accelerates aging in male mice Scientists at Dalian Medical University generated mice with liver‑specific knockout of 🔗 Read original →

Aberrant STMN2 RNA Found at Synapses in Frontotemporal Dementia Patients Researchers from the Barrow Neurological Institute in Phoenix examined synapses from 10 deceased patients with frontotemporal dementia (FTD) linked to a C9ORF72 repeat expansion and 10 healthy donors, also generating neurons from patient‑derived stem cells. They discovered that faulty RNA arising from TDP‑43 dysfunction, previously seen mainly in the nucleus, can accumulate at the synaptic junction — the point of contact between nerve cells. Aberrant STMN2 RNA was detected in synapses of 8 out of 10 FTD patients but in 0 out of 10 healthy donors; a cellular model of the mutation did not reproduce this defect. In the same samples, KALRN RNA appeared sporadically in synapses without a clear patient‑vs‑control difference, while UNC13A RNA was present in whole brain tissue of all patients but absent from synapses. Normally, TDP‑43 helps excise cryptic exons during RNA processing; its loss leaves these exons in the transcript, damaging the resulting protein. Neurons routinely transport RNAs such as healthy STMN2 to distal axons for local protein synthesis, and the aberrant copy likely follows the same route to the synapse. In the cellular model, synaptic protein density declined and network electrical activity weakened over weeks, indicating deteriorating contacts — a contrast to ALS models with the same TDP‑43 pathology, where neurons become hyperexcitable, reflecting the different neuronal populations affected (motor cortex vs. frontal cortex). Because the synapses were isolated from postmortem brains, they represent survivors; the state of lost synapses cannot be assessed. Current therapies aim to return TDP‑43 to the nucleus, and this work adds the synapse as a relevant target, given that a portion of the aberrant RNA reaches that compartment. 🔗 Read original →

Transplanted Heart Adopts Recipient's Biological Age, Not Donor's The preprint from Vadim Gladyshev’s lab shows that a transplanted heart quickly “forgets” the donor’s age and takes on the recipient’s biological age, as measured by epigenetic clocks; a young heart in an old body ages rapidly, while an old heart in a young body rejuvenates, and the recipient’s own heart, liver, and blood remain unchanged. Data from archival biopsies and clinical records of hundreds of patients confirm that graft age predicts the recipient, not the donor; on 25 September Yuri Deygin and Antonio Regalado reacted independently to the finding, each interpreting it through their own lens. Deygin saw the result as confirmation of his “Strong epigenetic theory of aging,” arguing that DNA methylation marks form a rewritable program that tissues continuously adjust to the organism’s age, while Regalado, editor of MIT Technology Review since 2011, warned that continual replacement with young organs would not work because the graft adopts the recipient’s age. He noted that the organ‑replacement strategy is termed “replacement” in the field, including a roadmap in Aging Cell co‑authored by Gladyshev, and that if an old body ages any new organ, endless part swapping ceases to be a standalone rejuvenation path. The study’s authors frame their observation as a starting hypothesis — graft and body exchanging accumulated damage — while independent expert João Pedro de Magalhães suggested immune‑system involvement, and first author Jesse Poganik added that some aspects of biological age are likely reversible, others not. Regalado’s conclusion was not a surprise to the lab; Gladyshev had previously presented at ARDD 2025 that “age assimilation” appears in heart, ovaries, and fat tissue, and that one organ does not rejuvenate the organism due to surgical trauma and immune response, a pattern that also supports Deygin’s model, highlights the limits of organ replacement, and leaves open whether aging rate should be managed systemically or by repairing parts. 🔗 Read original →

Embryo tissue stretch creates electric field that guides cell behavior On 24 September 2026 Olga Lyraki and Elias Barriga from Dresden Technical University published a review that synthesizes discoveries from 2015–2025 into a unified model of how bioelectricity directs tissue growth and repair. For decades biologists debated whether tissues generate their own electric field or merely exhibit a side‑effect of cellular ion‑pump activity. The review clarifies that the field is an active signal, not a passive byproduct. Early assumptions held that measured currents in muscle, heart, and skin resulted from ion pumps, and experiments applied artificial fields externally without testing whether the tissue itself could produce the field. Because the same ion channels are required for both field sensing and cell motility, distinguishing “feels the field” from “simply moves” proved difficult for many years. Recent advances with voltage‑sensitive fluorescent reporters and genetic tools in embryos finally allowed researchers to separate these functions. These tools show that endogenous bioelectric signals are independent cues that direct cell behavior during tissue formation, rather than mere markers of metabolism. The source of the field was demonstrated in earlier work from the same lab on Xenopus embryos. During neural‑tube formation, neighboring cells elongate and draw together, stretching their membranes and opening stretch‑sensitive ion channels. The resulting ion flow generates an electric field that emanates from the tissue itself. This self‑generated field guides neural‑crest cells after they detach from the 🔗 Read original →

Transhumanists confront limits of immortality beyond losing loved ones A forum user named AlphynKing posted an essay on r/Transhumanism on 26 September that examines the standard transhumanist reply to the objection “you will outlive everyone you love.” He agrees that if immortality were available to all, this specific problem disappears, but argues that even then, everything else a person values would still vanish. He points out that favorite games’ servers would eventually shut down, beloved restaurants would close, and cherished clothing would wear out and tear, all due to the relentless increase of entropy — the second law of thermodynamics — which makes literal immortality impossible. This entropic decay, he says, underlies the loss of all external sources of meaning, even if death itself were abolished. The author links this view to the Buddhist idea of non‑attachment, noting that suffering arises from clinging to things that cannot last forever, not from mortality itself. He also traces a secular philosophical lineage to Bernard Williams’s 1973 essay The Makropulos Case, discussed in the Stanford Encyclopedia of Philosophy, which argues that eternal life would eventually exhaust all reasons to keep living. He then surveys possible transhumanist responses — altering psyche to make loss painless, erasing memories of attachments, betting on a perfectly tuned AI god, or transcending humanity — and finds each unsatisfactory. Finally, he clarifies that his argument applies equally to finite life, endorses extending lifespan to 150 years and curing cancer as worthwhile goals, criticizes the movement’s millenarian promises that technology will solve everything forever, and urges transhumanists to frame their ambitions more modestly. 🔗 Read original →

Dual‑layer microneedle delivers drugs to skin layers, reducing fibrosis in mice In the September 21 article authors tested a microneedle with two modules. The superficial hydrogel releases SRT1720, an activator of SIRT1, in the dermis, while the spiral grooves hold lipid nanoparticles carrying PGC1α mRNA for subcutaneous fat cells. In a bleomycin‑induced fibrosis model, fibroblasts in the dermis showed senescence signs and adipocytes in the fat layer lost lipid storage and adopted a myofibroblast‑like phenotype. This depth‑specific pathology guided the design of the dual‑cargo system. The hydrogel module alone reduced dermal senescence markers and collagen deposition; the mRNA module better preserved the fat layer and limited adipocyte‑to‑myofibroblast transition. When combined, the microneedle decreased dermis thickness and collagen deposition after two weeks, restored elastic fibers and subcutaneous fat, and shifted gene activity toward weaker inflammation/fibrosis and stronger fat metabolism. These results were compared to a mechanical control (needle without cargo) and to each module alone, confirming that the combined approach outperformed single treatments. The 2024 study by the same group had previously reported loss of fat cells and myofibroblast transition in this model, informing the separate targeting of dermis and subcutaneous layers. One injection thus enabled simultaneous intervention on two linked processes residing in different skin layers. 🔗 Read original →

Turning off fat‑tissue hormone Lsp2 extends fly lifespan 14–28% without hurting fertility A Chinese team knocked out the Lsp2 gene in Drosophila (two mutant lines, including a CRISPR knockout) and observed a 14–28% increase in median lifespan while fecundity remained unchanged; flies even laid more eggs on days 8–10 and retained resistance to starvation, oxidative stress and infection. The study appeared in Nature (23 September) alongside an independent paper by Fumiaki Obata’s group in the same issue; both works identify Lsp2 as a hub linking dietary protein, ribosomal protein synthesis and fly longevity. Normally, larval Lsp2 accumulates in the fat body as building material for the pupal cuticle. After a protein‑rich meal, adult Lsp2 synthesis rises 80‑fold within 7 hours, acting as an adipokine released into the hemolymph. Its expression is driven by the insulin/mTORC1 nutrient‑sensing pathway, but Lsp2 exerts a focused effect: it alters only 35 genes versus the 684 genes changed by broad mTORC1 activation. Lsp2 works by increasing phosphorylation of the translational brake 4E‑BP, which releases inhibition on TOP‑mRNA translation, causing the cell to overproduce ribosomal proteins beyond actual need. Disabling Lsp2 (via the two mutant lines) lowered this excess ribosomal protein synthesis, saving energy without compromising functional ribosomes; consequently, median life rose 14–28%. In double mutants lacking both Lsp2 and 4E‑BP, the longevity benefit vanished, confirming that Lsp2 acts through the 4E‑BP translational brake. Rapamycin, which also targets mTORC1, shows far less predictable outcomes: diet composition flips its effect from +5.4% to −51.3% median lifespan change. On the same food, rapamycin extends the life of wild‑type flies but shortens that of Lsp2‑deficient flies, whereas Lsp2 directly modulates 4E‑BP phosphorylation in vivo. Obata’s isotopic labeling experiments revealed that amino acids from larval diet persist through metamorphosis and become incorporated into adult Lsp2. Low larval protein keeps adult Lsp2 levels low, which is sufficient to promote longevity; thus Lsp2 stores a memory of early‑life nutrition. Together, the two studies converge on Lsp2 and the 4E‑BP translational brake as a nexus of diet, aging and lifespan. The authors propose that insect hexamerins such as Lsp2 may functional analogues of human IgG—a abundant serum protein whose B‑cell production is also mTORC1‑dependent and whose excess links to aging. Although 🔗 Read original →

Receptor FcγRIIb identified as gateway for toxic alpha‑synuclein in Parkinson’s Researchers have identified a neuronal receptor that allows the toxic alpha‑synuclein protein to 🔗 Read original →