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

Ruptured red blood cell membranes trigger new capillary growth via ATP In an article published on 25 September in Angiogenesis, cardiologists at the University Medical Center Mainz led by Katrin Schäfer showed that the hemoglobin‑free membrane of burst erythrocytes reprograms vascular wall cells and launches capillary growth. The signal comes from ATP released by the erythrocyte membrane, which activates two endothelial receptors. ATP binds the fast P2X7 receptor, sparking the inflammatory NFκB pathway, and the slow P2Y11 receptor, raising cAMP levels. Both pathways converge on the protein NR4A1, which dampens inflammation and switches on VEGF and PFKFB3 genes — the latter acting as a metabolic “switch” that drives vessel building. In experiments, contact with the membrane altered the activity of 113 genes within two hours, including VEGF. In a 3D model the treatment produced as many new vessel branches as VEGF itself and sped up cell division and movement; purified heme did not elicit this effect. Patients with peripheral artery disease — where leg vessels fail to grow capillaries — show a weaker response, but the existing drug rolipram (a PDE4 inhibitor that preserves cAMP) restores it to healthy‑donor levels. A clinical precedent exists with cilostazol, a PDE3 blocker that already eases walking pain in these patients. The condition’s prevalence rises sharply with age: 5.3% of 45‑ to 50‑year‑olds and 18.6% of 85‑ to 90‑year‑olds are affected in developed countries. VEGF, first isolated and named in 1989, is now a target for cancer and retinal therapies that inhibit it. The findings suggest that an age‑weakened vascular repair signal can be revived using already‑approved drugs, without waiting for new compounds. 🔗 Read original →

Single-cell atlas reveals molecular similarities among Alzheimer’s, Lewy body, vascular dementia and Parkinson’s The PsychAD consortium built a single‑cell atlas of gene activity in the dorsolateral prefrontal cortex, profiling 6.3 million nuclei from 1494 donors ranging from newborns to 108 years old, including healthy individuals and patients with eight brain diseases. The atlas was published in Nature on 23 September. Choosing the same cortical region for all diseases makes the results directly comparable to each other and to earlier genetic data, explained project lead Panos Russos of the Icahn School of Medicine at Mount Sinai. Earlier single‑cell studies usually focused on one disease in a small sample and could not separate a general disease background from disease‑specific changes. After subtracting a common signal shared by all eight conditions — genes involved in protein assembly and transport — Alzheimer’s disease, Lewy body dementia, vascular dementia and Parkinson’s disease proved molecularly closer to each other than to schizophrenia or bipolar disorder. The authors also found that pairs of diseases with a higher shared genetic risk (based on genome‑wide data) showed more similar 🔗 Read original →

Lawsuit Seeks FDA Response on Petition to Classify Aging as a Disease On September 16, 2026, Ali Afshar filed a lawsuit in the U.S. District Court for the Southern District of New York against the FDA and its acting commissioner Kyle Diamantás, seeking to compel the agency to finally respond substantively to a 2024 citizen petition asking that aging be recognized as a disease, a request the FDA has not addressed for over two years. The suit was filed on behalf of the initiative Age Reversal Unity, which has pursued this recognition since 2024; the case received docket number 1:26-cv-08147 and Afshar paid the $405 filing fee himself, after which the court issued a summons. While the court cannot declare aging a disease, it can, under the Administrative Procedure Act, order 🔗 Read original →

Oracle Grants Buck Institute Access to 122+ Million Records for Aging Metric THRIVE On September 23, 2026, Oracle announced a partnership with the Buck Institute for Research on Aging to provide access to its de‑identified longitudinal health data for the federal THRIVE program aimed at measuring aging. The Buck Institute will receive 122+ million patient records from Oracle Health Real‑World Data, together with the Oracle Life Sciences Data Intelligence analytics environment. These data will support the THRIVE consortium’s work on the Intrinsic Capacity metric, which combines mobility, cognition, psychological health, sensory function, and physiological reserve into a single score of independent living ability. The metric is useful for aging‑intervention trials only if early changes in the score predict later outcomes such as frailty, chronic disease, hospitalization, loss of independence, or death. Demonstrating that predictive link requires years of real‑world histories, which the Oracle partnership supplies, allowing researchers to trace which early clinical signals precede deterioration. ARPA‑H, which funded THRIVE with up to $34.5 million in February, aims to predict such outcomes within about three years instead of waiting decades for traditional endpoints. Using the hosted Life Sciences Data Intelligence platform, Buck scientists can build cohorts, run queries, and perform bioinformatic analysis without preparing separate datasets. The first validation step—checking which combinations of historical features truly precede health decline—will be carried out on the 122+ million‑record set, after which the metric can be tested in clinical trials. 🔗 Read original →

Rad23b acts as double agent in Huntington’s disease, tagging mutant huntingtin while impairing proteasome In Huntington’s disease, the protein Rad23b works as a double agent: it enhances ubiquitin tagging of toxic huntingtin and simultaneously disrupts the proteasome that should destroy it. Taiwanese biologists reported on 24 September that the regulatory microRNA miR-196a lowers Rad23b levels. In cell experiments this reduced mutant huntingtin aggregates; conversely, extra Rad23b in mice increased them. Huntington’s disease arises when a DNA repeat expands in the HTT gene, producing huntingtin with an abnormally long glutamine stretch that forms neuronal aggregates. Cells normally label unwanted proteins with ubiquitin for delivery to the proteasome, which cuts them apart. Although miR-196a had been linked to fewer aggregates, its target gene was unclear because HTT lacks a binding site for this microRNA. The authors compared proteins in nerve cells with and without miR-196a; from 2681 detected proteins they shortlisted six candidates and confirmed two. For Rad23b they verified direct binding: mutating its RNA segment abolished miR-196a’s suppressive effect. Rad23b shuttles ubiquitin‑tagged proteins to the proteasome. In experiments Rad23b bound mutant huntingtin and increased its ubiquitin load, yet it also reduced the proteasome’s chymotrypsin‑like activity—one of its protein‑cleaving reactions. Consequently huntingtin became more heavily tagged but still accumulated. Knocking down or inhibiting Rad23b lowered aggregates; a proteasome blocker restored them, whereas an autophagy blocker did not. The same pathway was tested in Huntington’s disease model mice. Additional Rad23b worsened motor‑test performance, increased mutant huntingtin aggregates in the brain, and raised markers of neuronal death. In an independent dataset, Rad23b RNA levels were higher in lab‑grown neurons derived from symptomatic patients than from asymptomatic carriers of the same mutation. The authors suggest Rad23b’s role depends on aggregate type, citing prior work on C9ORF72‑related diseases where Rad23b gets trapped in other protein clumps and restoring its level reduces them. For huntingtin aggregates they propose a model where Rad23b stays bound to the cargo while weakening proteasome activity, so the ubiquitin tag no longer guarantees clearance. Huntington’s disease was first described by American physician George Huntington in 1872, observing three generations of a family; more than 150 years have passed without a disease‑slowing drug. In July Roche halted the tominersen trial: the agent lowered mutant huntingtin in cerebrospinal fluid but after 16 months patients’ movement, cognition and independent living did not differ from placebo. The new finding explains why merely lowering huntingtin amount may be 🔗 Read original →

Gene activity atlas reveals three lifespan phases and loss of daily neuronal rhythm after 60 Researchers from the PsychAD consortium analyzed gene expression in 1.3 million cell nuclei from the dorsolateral prefrontal cortex of 284 neurologically healthy donors ranging from birth to 97 years old. The tissue samples were used to create an atlas of transcriptional activity across the lifespan. The work was published in Nature, 23 September. In childhood and adolescence, the activity of 8223 genes changed with age, and more than 80% of those genes were expressed in neurons. Around age 24, the proportions of different cell types stopped shifting markedly, indicating a transition to a more stable cellular composition in this cortical area. During young and middle adulthood, only 27 genes and later a single gene showed age‑related expression changes. After age 60, age‑related changes resumed, with 735 genes altering their expression, and approximately 60% of those genes functioning in glial cells that support and protect neurons. The daily rhythm of gene expression also deteriorated: while dozens of neuronal genes cycled in concert between ages 20 and 59, only one neuronal gene retained such rhythm after 60. In older glia, emerging oscillations were linked to genes involved in response to misfolded proteins, a sign of cellular stress. Among the glial genes changing after 60, enrichment for Alzheimer’s disease‑related risk variants exceeded random expectation. The authors replicated the pattern in an independent cohort of 306 donors and confirmed it with tissue slices from four age groups. They suggest that future interventions should target the cell types and life stages where these transcriptional shifts are most pronounced. 🔗 Read original →

C5R’s AI‑run lab shows top model solves less than half of real science tasks C5R built Facility‑0, an AI‑managed laboratory, in 12 weeks. The system selects the next experiment, operates some instruments directly, and gives step‑by‑step instructions to human technicians for the remaining steps. A model receives a scientific goal — such as synthesizing a compound or reading a spectrum — then studies inventory, designs an experiment in code, translates that code into equipment commands and human‑readable directions, and after each run evaluates the results to decide what to try next. On 24 September the company released SciUniverse Level 1, a benchmark of 92 tasks spanning chemistry, biology and materials science — from organic synthesis and PCR DNA amplification to pressing ceramic tablets. The leading model, Claude Fable 5.1, succeeded on 45.3% of attempts on the first try, while the other five tested models scored lower. During testing the model controls instruments, lab staff and the reagent warehouse as a single agent, a fact confirmed by an independent audit of the system. After each experiment it reads measurements, plans the next move while respecting limited reagent supplies and prior outcomes. C5R says earlier AI‑in‑science evaluations only examined data after experiments were done, missing the full workflow of material selection, instrument operation and troubleshooting. SciUniverse closes that gap by measuring the entire chain from goal to outcome, including both physical runs in Facility‑0 and simulations on a digital twin of the lab using real experimental data. Models generally handle experimental strategy and calculations but often fail on manual details: pipetting frozen samples, vortexing open well plates, reusing a single pipette tip for multiple DNA wells (cross‑contaminating samples), and ignoring solvent evaporation during long reactions. Founder Michael Akilian previously worked on wearable electronics at Apple and Misfit Wearables, then founded and sold the AI‑scheduling startup Clara Labs. About eighteen months ago he shifted to experimental biology, building a worm lab in his apartment before joining a UC San Francisco laboratory, saying “Models succeeded in the virtual world but fell 🔗 Read original →

Second Lawsuit Challenges FDA Over Aging-as-Disease Petition This is the second lawsuit filed against the FDA regarding its demand to recognize aging as a disease. The first suit, filed about a year ago, was dismissed on a technicality—the missing signature—without addressing the substantive issue. Now a scheduling order has been issued. The core complaint is simple: the agency is ignoring a civil petition to classify aging as a disease that was submitted on 22 May 2024, demonstrating silence for more than two years. Let’s be clear: the odds that the FDA will tomorrow, under judicial pressure, concede and label aging a pathology are essentially zero. A Federal court lacks the authority to make medical decisions for a specialized agency. Under the Administrative Procedure Act, the most Afshar can achieve is to compel the bureaucratic machine to issue some official response—whether a denial, an agreement, or a defined timeline. Most likely, the FDA will simply reply with a boilerplate statement about “multifactorial natural processes,” thereby closing the procedural matter. Nonetheless, such lawsuits have concrete value. Each procedural clash, even if lost, generates informational noise, forces the system to react, and gradually shifts the Overton window. By repeatedly creating precedents and documenting regulatory obstruction in the public sphere, transhumanists turn radical life extension from a sci‑fi fringe topic into an inevitable public discussion. 🔗 Source: @solid_state_humanity

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Mitochondrial transplant reverses heart aging in mice via HIF‑3α/BNIP3 switch Researchers at Shanxi Medical University in China transplanted healthy mitochondria into the hearts of aged mice and found that the procedure restored cellular energy and pump function. They identified a molecular switch that drives the breakdown of mitophagy in aging hearts. The findings were published Aging Cell, 23 September 2026. In older hearts, the protein HIF‑3α shifts to a full‑length form that activates BNIP3, causing an overload of damaged mitochondria that cannot be cleared 🔗 Read original →

This is the second lawsuit filed against the FDA regarding the requirement to recognize aging as a disease. Officials dismissed the first lawsuit a year ago due to a simple lack of signature, without ever getting to the point, but now a subpoena has been issued. The gist of the complaint is simple: the agency is ignoring a citizen's petition to recognize aging as a disease, dated May 22, 2024, and has demonstratively remained silent for over two years. Let's get this out of the way: the chances that the FDA will cave under the judge's hammer tomorrow and declare aging a pathology are slim to none. A federal court has no authority to make medical decisions for the agency in question. The only thing Afshar can achieve under the Administrative Procedure Act is to force the bureaucratic machine to issue some kind of official response: a refusal, an agreement, or a specific deadline. Most likely, the FDA will simply issue a boilerplate statement about "multifactorial natural processes," closing the procedural matter. But such lawsuits have a concrete benefit. Every such legal battle, even one lost procedurally, creates information noise, forces the system to react, and gradually shifts the Overton window. We can't breach this wall in a single blow, but by constantly setting precedents and documenting regulatory sabotage in the public arena, transhumanists are transforming the topic of radical life extension from a fantasy fantasy into an inevitable public debate.

Frozen trial blood hints that drugs may already be slowing aging On September 24, biological‑age researcher Christine Gloriozo published an analysis showing that most drug trials collect and store participants’ blood but rarely test whether the treatment slowed aging. She examined two cases where such a check was done retrospectively — semaglutide and the experimental antifibrotic drug rentoceritib (a TNIK inhibitor from Insilico Medicine) — and found that aging clocks indicated a slowdown in treated patients. In the semaglutide trial of 108 participants with HIV, 84 retained samples were available for aging‑clock analysis. Using 17 clocks, the PhenoAge score showed the semaglutide group was on average 4.9 years younger than placebo, while DunedinPACE indicated a 9% slowing of aging pace. The effect was not uniform across all clocks, but seven of eleven organ‑system clocks showed significant slowing, including brain, heart, kidney and liver — a pattern unlikely to be random noise. Among the seven paper authors, two are employees and one is a consultant of TruDiagnostic, the developer of the epigenetic clocks used. The second example Gloriozo cites is rentoceritib, where six proteomic clocks from archived Phase IIa serum consistently showed reduced biological age in treated patients. She notes that publishing null results is also important: in the RAPA‑EX‑01 trial (rapamycin plus exercise) none of four clocks showed significant slowing. Separately, another study applied protein‑based aging clocks to five semaglutide trials involving 10,052 participants and observed the same slowing effect. Re‑analyzing stored blood from completed trials is a low‑cost way to build evidence that regulators might eventually accept aging‑clock slowing as a basis for drug approval. Each uns analyzed trial in a biobank represents a paid‑for but unasked question about aging. 🔗 Read original →

Gene therapy delivering Hsp70 extends lifespan in ALS‑model mice Russian researchers administered a single injection of an AAV vector carrying the human Hsp70 gene to mice with an ALS‑like condition caused by a FUS mutation. At the high dose, median survival increased from 128 to 170.5 days and the symptomatic stage was lengthened by 30% (18.7 days vs 14.4 days). Treatment began at day 58–60, when aggregated FUS had already accumulated in motor neurons, so the onset age of symptoms did not shift. Average lifespan rose by 23% at high dose, and the AAV vector remained active in brain and spinal cord for at least 150 days. Hsp70 works as a chaperone that refolds misfolded proteins and dissolves toxic aggregates; mutant FUS fails to fold correctly and forms clumps that overwhelm the cellular quality‑control system. Hsp70 levels fall with age and neurodegeneration. The preprint, 21 September showed that the 🔗 Read original →

Body‑Conductive Network Enables Millimeter‑Scale Implants for Health Monitoring Traditional radiofrequency standards such as Bluetooth and NFC penetrate biological fluids poorly and require bulky antennas and large batteries. The new approach uses the body itself as a conductor, sending ultra‑short electrical pulses that do not damage surrounding tissue, allowing distributed sensors and actuators to operate as a single autonomous network. By eliminating radiofrequency modules, implant dimensions shrink to less than 3 millimeters, enabling delivery deep into tissues or the stomach with a standard syringe and no major surgery. Each device consists of passive electronic components that consume virtually no power in standby and activate instantly upon receiving an impulse of specific voltage and duration. In experiments, a microactuator triggered once per day operated for about one year on an autonomous battery. The system, dubbed SWANS, was demonstrated on a rat locomotion‑synchronization model where a sensor detecting fore‑limb movement sent a signal through bodily tissues to an implant in the hind limb, eliciting precise muscle contraction and mimicking natural gait. The SWANS network is designed to transmit only minimal data—key triggers and activation commands—while complex computations are offloaded to an external wearable hub. 🔗 Read original →

Pancreatic alpha cells switch to insulin production when m6A lock is removed On 18 September 2026, researchers at the Joslin Diabetes Center of Harvard Medical School reported that the enzyme METTL14 maintains the specialized state of pancreatic alpha cells. When the METTL14 gene was deleted specifically in alpha cells of mice, some of those cells began to produce insulin instead of glucagon. The team traced the effect to a single nucleotide in the RNA of the YY1 gene, showing that the same regulatory node operates in human pancreatic cells. In the islet, beta cells secrete insulin to lower blood glucose, while alpha cells secrete glucagon to raise it. Earlier work in 2010 by Pedro Herrera’s laboratory in Geneva had demonstrated that after near‑total loss of beta cells, mouse alpha cells can start making insulin, but the factor that prevents this conversion in a healthy organ was unknown. The new study identified that brake: the METTL3/METTL14 complex deposits the m6A chemical mark on alpha‑cell RNA, and the level of this mark fluctuates with nutritional cues. Amino acids such as L‑arginine and low glucose stimulate glucagon release and, in a dose‑dependent manner, increase METTL14 and m6A; insulin and palmitate reduce the mark, whereas METTL3 showed little response in these experiments, focusing further work on METTL14. Deleting Mettl14 only in mouse alpha cells abolished glucagon secretion in response to amino acids, reduced alpha‑cell mass, and increased beta‑cell mass. The newly insulin‑producing cells retained an alpha‑cell lineage label, indicating they arose by direct conversion in situ, without transplantation or organ injury. A parallel experiment targeting the ALDH3B2 gene in pancreatic duct cells activated the insulin gene only after those cells were cultured outside the body and transplanted under the kidney capsule of diabetic mice. Single‑nucleus sequencing revealed that the conversion is incomplete: the cells lose alpha‑cell genes, gain insulin‑related genes, but retain immaturity markers, which the authors describe as progression toward beta identity rather than a finished state. By mapping m6A‑marked RNA regions against factors altered upon METTL14 loss, the authors pinpointed YY1 as the sole m6A target. Without the m6A mark, the YY1 transcript is degraded more slowly, leading to protein accumulation; a point mutation at the modified nucleotide confirmed this mechanism directly. Elevated YY1 suppresses alpha‑cell identity genes PAX6 and MAFB and activates growth pathways similar to those seen with METTL14 loss; both excess and deficiency of YY1 disrupt identity, showing it acts as a dosage‑sensitive regulator, not a simple switch. Analysis of 🔗 Read original →

CerS6 enzyme drives kidney podocyte aging via C16 ceramide–p53 pathway Scientists identified the enzyme CerS6 as a trigger of aging in kidney podocytes, the cells that form the blood‑filtering barrier, and showed that disabling it in mice slowed age‑related kidney damage. The findings were posted as a preprint on Research Square, 21 September 2026 by a team from the University of Texas Health Science Center at San Antonio, which demonstrated that CerS6 in podocytes promotes aging through the accumulation of C16 ceramide and activation of the p53 protein. In aged marmosets (~16 years) the CerS6–C16 ceramide–p53 pathway was more active than in young animals (~3 years), and mice with podocyte‑specific CerS6 knockout exhibited markedly weaker signs of kidney aging. Podocytes wrap the glomerular capillaries and do not divide, so loss of these cells irreversibly weakens the filtration barrier. Chronic kidney disease affects 38% of people over 65, and podocyte aging is one of its mechanisms. The researchers studied marmosets—New World primates whose genome was sequenced in 2014—as an aging model. Aged animals showed more senescent cells in glomeruli, higher p53/p21 levels, increased CerS6 and C16 ceramide in podocytes, and a correlation between higher CerS6, greater 🔗 Read original →

New PET tau‑reading system works with four tracers and detects early Alzheimer’s up to 2.7× more often The HEAD study, published on September 21, evaluated a new five‑class tau‑PET severity scale in 681 participants who received two to four scans with different tau tracers. Three physicians read the images independently, blinded to each other’s scores and to patient data. The regulator‑approved “yes/no” test works only with flortaucipir and is deliberately specific, which causes it to miss early disease. In comparison, the new scale identified 1.9–2.7 times more tau‑positive cases among cognitively normal individuals and 1.2–1.4 times more among those with mild impairment, while results converged at the dementia stage. Development of the method was led by Tariq Pascoal and Suzanne Baker, supported by the US National Institute on Aging with $41 million over five years. Earlier work showed that the MK‑6240 tracer is twice as sensitive as flortaucipir, though each tracer has a distinct binding profile preventing direct comparison. Amyloid PET already uses a common scale; the FDA approved a unified amyloid‑PET scale in August. Tau spreads predictably from deep memory structures to neighboring cortex. A normality threshold was set using scans of fifty amyloid‑negative healthy volunteers across all four tracers. The brain was divided into seven zones ordered by involvement, yielding the five classes: negative, low, moderate, high, and atypical. A free web tool guides readers through the zones and assigns the class; different readers and tracers gave highly concordant ratings. Cases flagged positive only by the new scale showed higher amyloid burden and elevated blood p‑tau217, confirming they represent early pathology rather than false positives. Memory test scores remained stable between negative and low classes but then declined stepwise: 2.5–3.3 points from low to moderate and another 4.4–4.6 points from moderate to high. As Pascoal stated in May, “Tau is the biology most tightly linked to symptoms and future decline. Finding tau earlier and staging it more precisely lets us identify who truly follows an Alzheimer’s trajectory — critical for trial enrollment now and for clinical decisions when new therapies emerge.” 🔗 Read original →

Physical resilience linked to slower kynurenine rise in older adults US and Dutch scientists released a preprint on 21 September describing a 28-year observation of the Rancho Bernardo Study cohort. They measured 22,736 molecules in serum from three visits of 237 participants and related the data to grip‑strength and chair‑rise speed as markers of physical resilience. A statistical model singled out 2,810 molecules associated with resilience from the full panel. Medium‑chain acylcarnitines — carriers of fatty acids into mitochondria — were higher in the low‑resilience group, signalling incomplete fat oxidation, whereas phosphocholines, lipid components of cell membranes, were elevated in those who maintained strength. Among five tryptophan derivatives, only kynurenine showed a different age‑related trajectory between groups: it rose more steeply in participants with low resilience at every visit. In a parallel experiment, activating the OR10J5 receptor in old mice drove mitochondrial growth and restored grip strength to youthful levels. Checking the acylcarnitine signatures against the tissueMASST database showed they are significantly 🔗 Read original →

Organ‑System Divergence in Routine Check‑ups Predicts Mortality Risk Researchers at Zhejiang University built an aging atlas from routine health check‑ups of 189 095 Chinese adults, compiling 94 055 326 measurements of 99 biomarkers across ten organ systems. For 147 492 of these participants, follow‑up mortality data were available, recording 4 599 deaths over the observation period. The analysis showed that the average deviation load across all systems predicted mortality, with each incremental step raising the risk of death by 5,8%. Greater instability between successive check‑ups increased mortality risk by 19% per step, and the effect was almost 1.5‑fold stronger for cardiovascular deaths, though it weakened after stricter statistical correction. Using the same data, the team trained a neural network called DynLifeNet that forecasts seven future health problems—such as kidney dysfunction, high uric acid, hypertension, glucose and cholesterol disturbances, anemia, and liver‑enzyme elevation—one to three years ahead. The model achieved an accuracy of 0,80 (versus 0.5 for random guessing), and adding organ‑system decomposition gave a small but statistically significant boost over baseline measurement history. Validation in an independent cohort of 16 478 participants from another long‑term Chinese study confirmed the relative importance of the organ systems, although the absolute risk scale did not transfer directly. 🔗 Read original →