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

OpenAI Foundation allocates over $125 million for health‑AI data projects OpenAI Foundation — the nonprofit parent of OpenAI — launched its second scientific initiative, Public Data for Health, and awarded the first tranche of **over $125 million 🔗 Read original →

AI model using routine data improves lung cancer immunotherapy outcome prediction On 13 September, Nature Medicine published work of the I3LUNG project analyzing 2,396 patients from six clinical centers. Authors checked whether an AI prediction based on routinely collected pretreatment data could outperform standard biomarkers and change the assessment of completed cases. Immunotherapy helps the immune system attack tumors, yet in metastatic non‑small‑cell lung cancer it is hard to know who will achieve disease control and who will live longer. PD‑L1 tumor level is one guide but captures only part of the patient’s situation. The study examined how much prognostic information already exists in ordinary medical records. For the main model the authors selected nine pretreatment features: sex, smoking status, ability to perform daily activities, PD‑L1, metastasis location, and blood‑test results. In an independent patient cohort the model surpassed single biomarkers and the LIPI blood‑based index in distinguishing disease control and several survival outcomes. Adding CT scans and digital tumor‑slice images improved performance when tested on data from the same centers, but this advantage was inconsistent in external groups. The model relying only on clinical data and blood work proved more stable, and the most reliable prediction came from the pretreatment data set that physicians already have. To test usability, twenty physicians reviewed 100 case histories, first with patient data alone and then with model output and explanations of which features shifted the prediction. After the model’s suggestion, correct identification of cases where disease was kept under control rose from 0.72 to 0.87, and overall accuracy increased from 0.57 to 0.65, although false‑positive control predictions rose slightly. The next phase of I3LUNG is already underway, testing the system on more than 2,000 patients. The published paper describes its retrospective phase—analysis of accumulated clinical data and review of finished cases together with clinicians. 🔗 Read original →

ProtScape ranks Parkinson’s drug targets far ahead of previous model ProtScape is a model that builds separate protein‑interaction maps for 207 cell types and states; it was released as a preprint on bioRxiv, September 14. To test target discovery, the authors hid 18 hidden Parkinson’s drug targets during training; ProtScape placed all of them within the first 511 ranks, whereas the earlier PINNACLE model required 8,186 ranks to achieve the same coverage. Unlike a generic interaction map that blends signals from many tissues, ProtScape constructs context‑specific networks using only proteins whose genes are active in each cell type, then predicts additional links by matching a protein’s amino‑acid sequence to its neighbors in that network. In the validation step, some links were removed from the original maps and the model reconstructed them from the remaining neighbors and sequence; each protein pair was assigned entirely to either training or testing data across all cell contexts, ensuring novelty for the test set. For 15 diseases, target rankings were trained using drugs with completed phase‑II human trials or stronger clinical evidence as positives; the ranking depth shows how many proteins must be examined to reach all 18 Parkinson’s hits: 511 for ProtScape versus 8,186 for PINNACLE (about a 16‑fold difference). After applying a preset threshold to unlabeled proteins, the authors obtained 102 candidates for follow‑up experiments. 🔗 Read original →

Guide RNA length shapes base editor activity in human globin genes A preprint released on 13 September shows that the length of the guide RNA determines which nearby DNA letters a base editor can modify in human cells. The study focused on the beta‑ and gamma‑globin genes, where changing the guide length altered both editing efficiency and the pattern of nucleotide changes. In the beta‑globin region targeting the HbE mutation, the desired change occurs at nucleotide A9 while the adjacent A10 can generate the Hb Aubenas variant. With a 15-nt guide, A9 was edited most frequently and the ratio of A10 to A9 edits was about ~3%. For the gamma‑globin target, the shortest guide length that yielded detectable editing depended on how the editor was delivered. In HUDEP‑2 cells that continuously produced the editor, a 15-nt guide gave measurable editing, whereas after transient delivery in HUDEP‑2 and primary progenitors editing began only with a 17-nt guide. Because the globin genes are similar, Cas9 can cut both sites, a situation linked in the group’s 2024 work to large deletions between them. PCR assays for the deletion products did not detect the expected fragments when using guides of 15–16 nt, and a nickase version (dABE8e) gave higher editing frequencies than the standard ABE8e with a 16‑nt guide. 🔗 Read original →

Mitchell McLennan calls pre‑birth PCSK9 editing an inheritable choice Mitchell McLennan made the comment on ** 🔗 Read original →

Preprint links P5 DNA site to Rep/Cap fragments in liver 🔗 Read original →

Lund University Starts Microelectrode Brain Stimulation Trial for Parkinson's On **September 1 🔗 Read original →

Consistency metric selects cases for autonomous AI diagnosis On 15 September Nature Medicine published a study of a locally deployed diagnostic AI agent. Researchers ran the same simulated clinical case five times and compared the meaning of diagnoses. Using a consistency threshold of 0.90, they allowed 272 cases of 551 cases for autonomous processing in the main configuration. The simulations used MIRA‑v2, a set of de‑identified patient records from MIMIC‑IV. In each case the doctor‑agent interviews a patient‑agent, requests permitted tests, and issues a diagnosis with explanation, all on local hospital infrastructure. In June MIRA turned the “diagnose from description” task into a multi‑step virtual chart encounter where the agent asks questions, orders studies, and picks a plan. For each of the 551 cases the team made five independent runs to capture variability. They defined ConsistencyDx as the agreement among the five diagnoses; it outperformed the model’s internal word probability (AUC 0.860 vs 0.747). When ConsistencyDx was at least 0.90, 272 cases went to autonomous flow, and 269 of those matched the benchmark label (98.9%); the remaining 279 cases were sent for physician review. A stress test that removed the patient‑history prompt dropped accuracy from 90.6% to 70.2% and lowered ConsistencyDx, while internal probabilities and linguistic confidence features stayed high. Five runs required roughly five times more tokens than a single run. On the external VivaBench set, ConsistencyDx remained the best metric; at a threshold of 0.85, 32.0% of cases were kept for autonomous processing with an accuracy of 89.9%. The optimal threshold must be recalibrated for each deployment because it depends on model, generation settings, number of repeats, and the method used to compare diagnosis meaning. 🔗 Read original →

Study identifies two MRI subtypes of Alzheimer's with distinct progression patterns On September 11, the preprint described two MRI‑based subtypes of Alzheimer’s disease that show different patterns of worsening. The authors combined baseline MRI scans from 1,396 participants across four North American research cohorts. Using the SuStaIn model (SuStaIn algorithm, 2018), they identified two statistical trajectories of change. One trajectory begins with atrophy of memory‑related regions (parahippocampal and temporal areas) followed later by growth of white‑matter lesion volume. The other starts with an increase in visible white‑matter lesion volume, especially in the occipital lobe, then expands ventricular spaces and shrinks memory‑related regions. Similar‑looking changes on a scan can belong to different disease stages, and standard MRI grouping often mixes trajectory type with stage. When the model was tested on ten data splits, two subtypes best explained the data. In both groups, amyloid and tau levels were abnormal. The subtype with early white‑matter lesions showed higher blood pressure and, in one cohort, a larger volume of enlarged perivascular spaces. The subtype with early atrophy had faster decline on memory, attention, language and global cognition tests. Among the 1,145 participants with clinical follow‑up, a model adjusted for age and sex linked early atrophy to higher odds of progressing to an Alzheimer’s diagnosis compared with early lesions. Future studies could use these two trajectories for participant selection and prognosis, as they are associated with different rates of cognitive decline. 🔗 Read original →

UK AI Health Commission Recommends Staged Approval and Post‑Launch Monitoring On September 10 the National Commission for AI Regulation in Healthcare published 44 recommendations for future UK rules on medical AI. The advice is directed to the UK Medicines and Healthcare products Regulatory Agency (MHRA), the government, and healthcare organisations. Medical AI can change after updates and perform differently in various clinics, with outcomes influenced by data, workflows, and conditions of use. In the current UK system safety and performance checks focus mainly on pre‑deployment data, while post‑market surveillance relies heavily on incident reports. According to recommendation 14, MHRA could initially authorise a device only under defined conditions of use — after reviewing initial data, risk‑mitigation measures, and reporting requirements. Later, the scope of use could expand if the system meets pre‑set safety and performance thresholds, with the temporary status made clear to patients and the path to full authorisation set out in advance. After launch the commission calls for mandatory monitoring plans, real‑world studies, and regular performance reports; if performance deteriorates an escalation procedure must apply. Another recommendation proposes inserting the device identifier and its version into the patient’s health record to help clinicians trace outcomes. The report also links safety to how a clinic adopts the technology, requiring manufacturers to describe safe‑use conditions — including user training and clinic readiness — and for contracts to allocate responsibility for these measures, with clinics tasked to train staff on the specific technology. 🔗 Read original →

Clarifying the Fly Brain Hype: No Consciousness in Bitcoin Trading Media hype surrounding the digital fly brain often mischaracterizes simple machine‑learning tricks as signs of consciousness. For example, making the model “trade” Bitcoin can be extrapolated to any other stunt — playing Bad Apple, solving a Rubik’s cube, or waving a lightsaber. Journalistic framings replace the technical process with anthropomorphic ideas like a “digital mind” or “conscious activity.” In reality, the fly connectome is not a functioning biological system nor a computational program; it is a static topological map of spatial connections among ~160,000 neurons and tens of millions of synapses. This graph itself lacks neurotransmitter dynamics, electrical activity, or subjectivity. Any manipulation using the digital model follows a single algorithm: input data are converted into a signal matrix that mimics visual or sensory neuron stimulation. To activate the static graph, it is embedded in external machine‑learning architectures such as Graph Neural Networks. Trading or key presses are executed not by the connectome itself but by an optimization model that uses the brain topology as a specific structured weight matrix. Meanwhile, the model’s dopaminergic and aversive neural circuits are forcibly stimulated: profit from a trade or gameplay advantage is supplied as a positive mathematical reinforcement signal. Understand? No fly is learning to trade or play poker. The procedure is a standard loss‑function optimization where the biological graph serves merely as an alternative connectivity architecture. Interpreting these experiments as steps toward “transferring consciousness” or “creating digitized intelligence” is inaccurate; they represent an engineering adaptation of biological data to applied machine‑learning tasks. 🔗 Source: @solid_state_humanity

Blocking ceramide synthesis pathways shows opposite effects on Alzheimer's symptoms in mice On 11 September, researchers published a bioRxiv preprint comparing two strategies to lower ceramide levels in the PDAPP‑J20 mouse model of Alzheimer’s disease. Eight‑month‑old female mice received either GW4869, which blocks the neutral sphingomyelinase (nSMase) pathway, or myriocin, which blocks the serine‑palmitoyltransferase (SPT) pathway, for three weeks. Mice treated with GW4869 learned the Barnes maze at the level of healthy controls, showed a reduced amyloid‑plaque area in one hippocampal region, and exhibited fewer signs of microglial activation around plaques. In contrast, mice given myriocin retained learning deficits and had a larger plaque area in that region compared with untreated transgenic animals. In microglial cell culture, amyloid induced NFκB nuclear translocation; GW4869 blocked this translocation and lowered intracellular fluorescent amyloid. A chemically distinct nSMase inhibitor, cabotin, decreased TNF‑α production but did not reduce intracellular amyloid in the same assay. Thus, the effect depended on the ceramide‑synthesis route: inhibiting nSMase with GW4869 improved learning and lessened amyloid burden, whereas inhibiting SPT with myriocin worsened some outcomes. 🔗 Read original →

Human brain circuits grown inside mice after cortex replacement Scientists genetically modified mice so that from birth they lacked almost the entire cerebral cortex, leaving only about 2% of normal cortical volume. Into this void they implanted laboratory‑grown human brain organoids in two‑day‑old newborn mice. After three months, more than 90% of the rodents’ cortical volume consisted of engrafted, functional human neurons that had integrated into the spinal cord and nervous system. The approach overcame past limits where human cells competed with mouse neurons for space. Each implanted organoid contained roughly 100,000 cells. With the freed niche, researchers were able to grow the rare spindle‑shaped von Economo neurons (VENs), which occur in the human brain at a frequency of about 1 per 90,000 neurons and are linked to social behavior and decision‑making. Previously VENs could only be studied post‑mortem, as they fail to form in petri dishes. This “xenocortical” model may aid research into neurological disorders. In additional tests, mice were subjected to a five‑hour oxygen deprivation, showing that the human tissue is many times more sensitive to hypoxia than mouse tissue and can provoke cerebral‑palsy‑like symptoms. The method will allow personalized organoids to be grown from a patient’s skin and used to test precise drugs directly on living neural networks. 🔗 Read original →

Paper2Agent turns papers into AI agents that apply methods to new data Paper2Agent takes a paper’s text, code, and data and builds an agent that can answer questions about the work and collaborate with agents from other papers. Applying a method from an article is usually locked behind technical 🔗 Read original →

Gene hoxb5a Determines Spinal Cord Regeneration Outcome in Zebrafish In zebrafish, a leading model for spinal cord regeneration, roughly one‑third of fish stay paralyzed after a complete cord transection even though the lesion tissue fuses in all animals. Researchers traced this variability to the gene hoxb5a, which decides whether regeneration succeeds or fails. The team analyzed 254 adult zebrafish with full transections in a Morgridge Institute preprint, September 14. After six weeks, 93 fish (28%) had not recovered swimming despite tissue fusion; the key difference was whether nerve fibers regrew to their original targets. Profiling of >60 000 nuclei from the injury site revealed identical cell types in all fish, but divergent programs: successful fish showed fibroblasts activating axon growth and guidance genes, while paralyzed fish deposited matrix fibers that block axons; immune profiles also differed, with more active T‑cells in the recovering group. Network analysis pinpointed hoxb5a as the most connected Hox gene in fibroblasts of successful fish. Mutant lines lacking hoxb5a saw the paralyzed fraction rise to 63% vs 13% and axon regrowth beyond the lesion drop from 70% to 14%; six other candidate genes produced no effect, indicating hoxb5a’s specific role in remodeling the extracellular matrix and signaling around fibroblasts. Zebrafish share this regenerative capacity with lampreys and salamanders, a trait absent in mammals, including humans. The discovery emerged from routine screening in the lab that first demonstrated zebrafish heart regeneration; the effect was consistent across batches, sexes, and surgeons, highlighting hoxb5a as an intrinsic switch that could potentially be harnessed to promote repair. 🔗 Read original →

HexemBio raises $15.5 million to rejuvenate blood stem cells, targets 2027 first‑in‑human trial HexemBio has secured a total of $15.5 million for a therapy that temporarily returns aged hematopoietic stem cells to a lab‑made copy of the embryonic yolk‑sac niche where they originate. The round closed on 15 September with new investor Happiness Capital joining existing backers Draper Associates and Boost VC. The same synthetic yolk‑sac niche under 🔗 Read original →

Frequent feeding cuts female killifish lifespan by a third, leaves males unchanged Researchers at the Medical University of Vienna built a low‑cost automatic feeder for turquoise killifish (Nothobranchius furzeri) and tested feeding frequencies from two to 36 feedings per day while keeping the total daily food amount constant. The species naturally lives only four to six months, making it a rapid vertebrate model of aging. Frequent feeding accelerated growth in both sexes, but female median lifespan fell from 21.9 to 15.1 weeks (≈30% reduction), whereas male median lifespan remained unchanged at 20–22 weeks. In a parallel experiment, vgll3‑edited males grew faster but lived 15% shorter. The feeder uses an Arduino‑controlled stepper motor and interchangeable tubes to dispense food with milligram precision, costing about ≈€500 per 100 aquariums. It was deemed cheaper and more accurate than existing commercial options. With fatty feeds such as Biomar and Otohime, females laid more eggs early but embryo survival dropped sharply, compressing the reproductive period 🔗 Read original →

Immortal Dragons Narrows Focus to Whole‑Organ Replacement Strategy Immortal 🔗 Read original →

Adult Drosophila thigh muscle rebuilds destroyed myofibrils in a week On September 15, biologists from Dalhousie University showed in a non‑peer‑reviewed preprint on bioRxiv how adult Drosophila thigh muscle recovers after severe damage. The muscle’s structure and mobility returned almost fully within a week. Damage was induced by expressing light‑ or heat‑sensitive channels and then exposing flies to red light or heating to 37 °C for one‑two hours, causing continuous contraction without surgery. Immediately after stimulation the flies were nearly paralyzed, but movement speed returned to baseline after seven days, regardless of damage method. Fluorescent Z‑disk markers showed that 50–60% of muscle area lost structure right away, but this proportion fell to zero by day three. Electron microscopy confirmed the Z‑disk spacing increased from 191 to 897 nm and returned to 187–191 nm after a week. The key player was the protein filamin, which sits on the Z‑disk and crosslinks actin filaments of neighboring sarcomeres, switching between open and closed forms under load. Flies with normal filamin developed mild damage by week two and severe damage by week three, while those locked in the closed form showed protein aggregates already by week one and impaired recovery. In 2024 the same lab showed filamin protects Z‑disks in wing muscle during contraction, but did not test whether muscle could rebuild myofibrils after severe destruction—this study answers that. Human filamin C mutations cause hereditary myofibrillar myopathies, linking the fly findings to 🔗 Read original →

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