VOICE Model


The VOICE model evaluates gene activity in individual cells based on tissue images and a library of already measured cells. On August 8, a team from the University of Michigan released the VOICE model preprint. The authors trained the model on 23.2 million cells from 75 human tissue sections across 15 tissues, where each cell has a standard H&E-stained tissue image and gene activity measurements using Xenium technology.


The model takes cell shape from the image and, for genes that cannot be recognized by shape, refers to a library of similar cells where gene activity has already been measured. H&E staining shows cell shape and tissue structure, while Xenium technology measures the activity of pre-selected genes in individual cells of the same section and retains their coordinates. The model was trained on sections where these two types of data were already matched.


The model has two paths to a single estimate: a direct path using H&E cell features and its surroundings to estimate gene activity, and a second path that searches the library for similar cells of the same tissue and averages their measured Xenium values. For each gene, VOICE adjusts the weight between these paths on the training sections. The authors describe this division as: "some genes are closely related to cell morphology and are predicted directly from the image; others are better evaluated by cells with a similar transcriptomic profile". The transcriptomic profile is a set of gene activity measurements in a single cell, as described in Nature Aging, July 2026.

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Matrix Proof Found


The GPT-5.6 model helped find a path to proving the 22-year-old Kroizë hypothesis on matrices. On July 27, Shangmu Jin posted a manuscript with an exact boundary for matrix functions. On August 14, mathematicians Alex Townsend and Anne Greenbaum reported that, along with the hypothesis author Michel Kroizë, they had thoroughly checked the proof.


The Kroizë hypothesis states that if a polynomial p, a formula of additions and multiplications, nowhere exceeds a magnitude M on the numerical range of a matrix A, then the matrix p(A) has a norm no higher than 2M. In 2004, Michel Kroizë formulated a general variant of the question, and his 2007 estimate gave a multiplier of 11.08; in 2017, Kroizë and Palenzia reduced it to 1 + √2, approximately 2.414.


To get exactly two, a different approach was needed in the proof. In the previous approach, the target value was estimated along with an additional expression, which kept the universal bound above two. The current manuscript by Jin cites a specific contribution from ChatGPT: the model suggested where to take the values of the auxiliary function and add a point at zero. This choice removes the additional expression, and comparing two weighted sums of squares gives a multiplier of two, as reported in SIAM News.

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Discovered Materials Test


Discovered Materials launched the Material Discovery Bench, a test for AI models searching for materials for multilayered microchips, on August 12. Seven models proposed 526 candidates, but only one recipe received a "worth trying" evaluation; the team is attempting to synthesize this material.

In such microchips, memory is placed on top of logical circuits to reduce signal travel distance. A dielectric is needed between layers to isolate electrical circuits and dissipate heat. Otherwise, accumulated heat within the assembly limits the number of layers.

The AI model searches for articles, works with materials science programs, and proposes a crystalline structure - a way to arrange atoms in a substance. Computer models select variants that, according to calculations, effectively dissipate heat, isolate electrical circuits, withstand load, and maintain structure, resulting in a calculated candidate for an interlayer material.

As reported in Nature Aging, July 2026, the model must then write a recipe for a thin film - a layer of substance deposited on a plate. The recipe must specify the starting substances, their application method, and the conditions under which the desired atomic arrangement is obtained. Specialists in thin film deposition evaluated recipe examples and developed rules; during the test, a separate language model applies these rules.

The team is now attempting to synthesize the single material that received a "worth trying" evaluation, following the Material Discovery Bench protocol.

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Biostasis Quality Criteria


The Biostasis Roadmap co-author, Emile Kendziorra, stated that two years after its publication, most tasks remain open. One of the questions is what degree of brain preservation is needed for future methods to restore a person. Biostasis is an attempt to preserve a person in anticipation of future medical advancements that could restore them. The focus is on brain structures related to memory, personality, and identity.


Developers need a criterion that shows which damages are still compatible with preserving this information. The Biostasis Roadmap 2024 authors described several levels of testing, including light microscopy, electron microscopy, and the arrangement of proteins, lipids, and nucleic acids, including DNA and RNA. After thawing, researchers can check cell viability and electrical activity of nerve tissue.


Computer tomography (CT) and measurements during the procedure provide indirect data, showing how the cryoprotectant - a solution that reduces ice formation - is distributed in tissues. These indicators are useful when their results are compared with the state of cells and tissue structure. In a new post, Kendziorra formulated the purpose of the roadmap as "a to-do list," and a general criterion would allow comparing different protocol improvements.

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Mice Study Reveals DLK1 Source


Researchers found that in mice with shortened telomeres, microglia is a source of DLK1, a protein that inhibits the maturation of myelin-producing cells. In an article published in Neuron on August 11, the authors separately investigated the source and action of the soluble form of DLK1, sDLK1.

In a telomere model, excess sDLK1 in the spinal fluid primarily came from microglia, and in other experiments, the protein itself delayed the maturation of myelin-producing cells. The authors bred mice without the Terc gene, necessary for telomerase enzyme function, for three generations.

In the third-generation mice, the telomere signal in microglia was lower, and microglia acquired signs of cellular aging. At the same time, there were changes in the gene function of oligodendrocytes, the cells that produce the myelin sheath around nerve fibers. A 2023 study had already shown that DLK1 of neuronal origin can delay the maturation of oligodendrocyte precursor cells.

The current authors investigated whether microglia with signs of cellular aging could be a source of the same protein. A July study had found inflamed microglia with signs of cellular aging near myelinated fibers in old mice. The current experiments tested one of the signals through which such microglia may affect myelin cells.

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Biological Age Linked to Gene Activity


A study published on July 20 in npj Aging analyzed 3,227 participants from the Health and Retirement Study, a long-term American study of people over 50 years old. The researchers measured both methylation, or chemical marks on DNA, and RNA levels, which indicate active genes in blood cells. Epigenetic clocks are formulas that convert DNA marks into an estimate of biological age, and they were trained to solve different tasks: Horvath and Hannum predict calendar age, PhenoAge and GrimAge predict health indicators and mortality risk, and DunedinPACE measures the pace of age-related changes in multiple systems.


The authors found that 49 genes were statistically associated with high Horvath values, while 3,204 genes were associated with DunedinPACE. No single gene was common to all five clocks, and the same result was obtained when comparing pathways in Reactome, a catalog of biological processes. On a broader level, the estimates converge, all affecting metabolism, development, immune function, and cellular regulation.


The researchers created transcriptomic aging signatures, TAGS, based on the profiles of genes associated with each clock. They were calculated based on RNA levels of genes associated with the corresponding clocks and were validated on 2,584 participants. The connection between TAGS and the corresponding clocks was moderate, reflecting current gene activity in the blood, while the original clocks reflected chemical marks on DNA. In a group of 645 people, TAGS were more strongly associated with several outcomes than the corresponding DNA methylation clocks.

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Mouse Aging Atlas


The mouse aging atlases show how tissues change the composition of cellular populations at different age windows. On August 14, Quanta Magazine published an interview with cellular biologist Junyue Cao about two mouse aging atlases. They allow tracking of how the proportion of different cellular populations in tissues changes with age and what signals accompany these transitions.

Tissue consists of cells with different tasks: some support vessels and tendons, others participate in the immune response, and others restore damage. With age, their ratio changes. Cao studies which populations shrink or expand in each age window and what signals are associated with these transitions.

He came to this task when searching for molecular targets to slow down aging: many molecular pathways are associated with age, and their action depends on the cell type. His group developed EasySci, a method that reads active genes in the nuclei of individual cells. By this set of genes, one can recognize the cell type and count how its proportion changes in the tissue. The PanSci atlas includes 21,786,931 nuclear profiles from over 600 samples of 14 tissues taken from mice of both sexes aged from three to 23 months.

All samples were processed according to the same scheme so as not to take differences between data batches for age-related changes. The authors found more than 200 cellular populations whose proportion in tissues changed significantly with age. Some groups shrank, others expanded; shifts occurred at different age windows. Nature Aging, July 2026, also explored this topic.

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New Sight Restoration


A new approach to "turning on" a blind retina without genetic operations or implants uses special light-sensitive molecules that work as a molecular prosthesis for dead photoreceptors. The most impressive aspect is that in animal experiments, it worked not only after injections but also in the form of ordinary eye drops, under room-level lighting. This technology targets diseases that destroy photoreceptors, such as age-related macular degeneration and retinitis pigmentosa. The new technology utilizes photopharmacology - prosthe6 molecules that change shape under visible light.

They attach to the mGlu6 protein on ON-bipolar cells, which normally receive signals from photoreceptors. When light enters the eye, prosthe6 is activated and triggers a signal chain, as if the photoreceptor were still working. This is maximally close to natural physiology. In animal experiments, the results were noticeable: blind fish regained rapid eye movements, which require complex image processing. Mice with models of macular degeneration and retinitis pigmentosa regained light-perception behavior, avoiding bright areas again.

The prosthe6-12 and prosthe6-15 versions worked especially well, with the effect appearing after injection and after drops, under ordinary white light, without special lamps. The molecules act at an early stage of the visual chain - on bipolar cells, not on deeper structures like electronic implants. This gives a chance to preserve natural image processing within the retina. However, it is currently impossible to say how detailed human vision will be: animal behavior shows the presence of light sensitivity but not the restoration of sharpness.

There are also first steps towards the clinic: in Australia, a small test of another photo-switchable drug, KIO-301, has already been conducted on 6 patients with severe retinitis pigmentosa, as reported in Nature Aging, July 2026. It was safe but not intended to test efficacy. This shows that the technology is already moving out of laboratories. The most promising aspect is the drop form: if it can be proven that the drug passes through the human cornea in the necessary concentration, treatment may become simple, without requiring surgery, implants, or special glasses.

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Neurons Revitalized


Researchers found that enhancing cellular cleanup in neurons derived from elderly donors' skin cells improved some mitochondrial metrics. On August 16, 2026, Eva Kliman and colleagues published a study on cortical neurons directly converted from skin cells of people of different ages. The neurons from elderly donors had weaker acidic stages of autophagy, a cellular cleanup process.


The authors increased the formation of autophagosomes, vesicles for this cleanup, and some mitochondrial metrics in the neurons from elderly donors approached those of young cells. The study was published in Nature Aging, July 2026. The researchers used G2-115 to increase autophagosome formation, resulting in a 60% increase in their number in all age groups.


The authors compared young and old cell lines, as well as six pairs of samples taken from the same men approximately 15 years apart. In the old cells, 16.64% of autophagosomes were acidic, compared to 47.06% in young cells. The results suggest that the lack of lysosomes in the neurites hinders autophagosome acidification, leading to more frequent mitochondrial division and fusion.

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Implant Generates Electricity


The implant is a thin, biodegradable film that dissolves in the body over time, but while it works, it can be powered by external ultrasound and glow under ultraviolet light, showing its status. The technology is based on the triboelectric effect, where two different materials come into contact and rub against each other, generating a static charge. Researchers embedded a molecule called Ir1b in a biopolymer, a luminescent material based on iridium, which they found and refined using machine learning.


The Ir1b molecule was found to be approximately 1.8 times more efficient than regular luminescent materials in generating a triboelectric charge. The size of one molecule is just 1.3 nanometers. When an ultrasound of 20 kHz frequency is directed at the implant, it starts generating electricity: up to 3.6 V voltage and around 16 μA current. This is enough to power simple biomedical functions.


The implant is almost invisible under the skin, but when exposed to a UV lamp, it starts glowing. In experiments on mice, the device's contour was clearly visible, and if the film was damaged, the glow disappeared, indicating that the implant was broken or displaced. This technology has potential, especially for devices like biosensors or drug delivery systems, where a battery can increase size, complicate design, and pose risks, as reported in Nature Aging, July 2026.

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DARPA Firefox Program


The DARPA agency has a program called Firefox, which is not related to the famous internet browser, but rather named after a cult film about a mentally controlled fighter jet. The program aims to create a non-invasive brain interface that can match the accuracy of implants without surgery or electrodes, using only optical methods. DARPA has set specific targets: 100 channels, spatial resolution of 50 microns, and temporal resolution of 100 microseconds.


This level of precision can read the activity of neural ensembles, not just general fluctuations. Currently, the agency has an optical system that can register signals at the depth of the human cortex, but it works on a limited scale. The Firefox program needs to solve two problems: quickly "scanning" multiple areas of the brain simultaneously and processing the massive data streams that will exceed the capabilities of classical digital electronics at such frequency and resolution.


DARPA explicitly states that it will be necessary to "exit the digital domain", which means searching for computational architectures that can work with neural streams in real-time, such as quantum circuits, neuromorphic processors, or even biocomputing. The idea is simple: if the interface must work at brain speed, then the calculations must be closer to its principles. Registration for the program is open until August 21, 2026, and the first day for developers is September 1.

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Cortisol Shifts Cell Clocks


The hormone cortisol sends a signal to cells to adjust their internal clocks, leading to a rapid increase in the production of the Per1 gene and PER1 protein. This process is crucial for synchronizing the cell's internal clock with the body's natural rhythm. Researchers found that cortisol, a glucocorticoid hormone, plays a key role in this process, and their findings were published in a preprint on August 13.


The study revealed that the glucocorticoid receptor, a protein that binds to cortisol and transmits its signal to the cell, is essential for this process. The researchers used a selective activator of the receptor to shift the cell's clock, and two receptor-blocking compounds to cancel this effect. They also found that disabling the receptor gene prevented the cell from responding to cortisol, but introducing an artificial variant of the receptor that is constantly present in the nucleus restored the response.


The researchers then focused on the Per1 gene, a key component of the molecular clock. They found that after a hormonal pulse, the level of mature Per1 RNA increased rapidly, and the level of PER1 protein increased within 12 minutes in human cells. The study also showed that this rapid response is due to enhanced RNA processing, rather than new RNA synthesis, and that it is mediated by the glucocorticoid receptor. The findings were published in preprint, August 2026.

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Insilico Launches Virtual Aging Cell


Insilico Medicine launched the Virtual Aging Cell page on August 14, providing a preview of the project the company is developing. The page features a demo screen with artificially generated data, where users can input the organism type, tissue, biological age, and substance to simulate a molecular response.


The Virtual Aging Cell is a computer model that builds a predicted molecular response based on the given conditions. The biological age is estimated from the cell's state data and may differ from the organism's calendar age. Insilico suggests using the Virtual Aging Cell to compare the predicted cellular response to a single intervention at different age states.


The company claims that the future model will generate three types of profiles: gene activity, protein composition, and DNA methylation. These calculations will help compare the predicted effect of a substance on tissue at different age states and select a hypothesis for the next laboratory experiment, as described in Nature Aging, July 2026.

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Alzheimer's Protein Tau

Researchers applied the STARFISH method to primary mouse neurons, detecting tau protein synthesis in dendrites, the branches that receive signals from other cells. A membrane-bound complex called the proteasome quickly degraded about a third of the new tau protein. When this complex was blocked in neurons and a mouse model with human tau, aggregates accumulated, depending on new protein synthesis.


In a healthy brain, tau is mainly concentrated in axons, the long extensions through which a neuron transmits signals. In Alzheimer's disease, some tau appears in the cell body and dendrites, where protein clusters form. The authors asked if some of this protein is born directly in the dendrites. A map of mRNA shows where the cellular instructions for assembling a protein are located. STARFISH shows the moment when a ribosome reads the instructions and assembles the protein.


In mouse neurons, the mRNA map of tau covered the cell body and extensions, while STARFISH detected active tau synthesis only in dendrites. A three-dimensional reconstruction separated the dendrites from intersecting axons. The authors labeled newly assembled tau for 30 seconds and tracked its fate, finding that almost half of the label disappeared within 30-60 seconds. The substance iBEp, which blocks the proteasome, stopped this rapid degradation, with the authors estimating that the proteasome degrades about a third of new tau.

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China Unifies Lab Test Pricing


The National Medical Insurance Administration of China released a trial guide on laboratory service prices on August 14. The document consolidates previous regional positions into 662 main tariffs, 114 surcharges, and 7 extensions. Provinces must determine a uniform base price level, and municipalities with pricing authority must set actual rates around it.


Previously, in most regions, the same test was paid for at different rates depending on the methodology. The new guide introduces a single price for a measurable indicator, regardless of technology: for example, a blood glucose test now has a single tariff instead of separate rates for different measurement methods. The payment amount now also depends on data preservation. In an official clarification, the agency introduced a rule: clinics are required to preserve and transmit analysis data and results to the system.


If a laboratory does not preserve and upload this information, the insurance payment for each indicator is reduced by 10%, but no more than 5 yuan. When researching multiple indicators in one analysis, the total deduction is also limited to 5 yuan. The regulator introduced this requirement for mutual recognition of analyses between different clinics and regions. To enable another doctor to use an already prepared result, a single number on the form is not enough: a reference interval - a range of normal values - is needed to compare the measurement.

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Model ESM-2 Accuracy


The compressed version of the ESM-2 model maintained average accuracy but severely distorted the ranking of substitutions in the UBR5 protein. On August 15, Cen Shao compared six computation modes for three ESM-2 versions in a preprint. The evaluation covered 201 laboratory measurements from the ProteinGym dataset on the effect of amino acid substitutions in proteins.


The ESM-2 model reads the amino acid sequence and ranks possible substitutions by expected effect. The laboratory can choose the top lines of such a ranking for the next experiment, so it needs an accurate order of variants for its protein. Shao ran 2.41 million variants through three ESM-2 sizes and six precision modes. In the 3 billion parameter model, 8-bit compression almost did not change the average correlation with laboratory measurements: the difference with full precision was −0.0021.


At the human UBR5 protein, the same correlation fell from 0.591 to 0.223. The average metric described the entire set of experiments, and the ranking of variants for one protein changed radically. The reason lies in the scoring method. The model receives a substitution score by subtracting the close logarithms of the probability of the original and new amino acid. A small compression error in each of these numbers after subtraction can become a noticeable part of the final difference and change the order of candidates. As reported in the ProteinGym dataset, such errors can significantly impact the results.

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Sprint Cycling Study


A recent study compared the effects of six 30-second maximum sprint cycling sessions with 90 minutes of continuous moderate cycling on the blood of 19 young men. The study, published in Cell Reports Medicine, August 13, measured proteins in the plasma, the liquid part of the blood, before exercise, immediately after, and three hours later.

The intense sprint cycling caused a rapid early shift in protein levels, while moderate cycling caused a smaller delayed shift. After exercise, muscles, fat tissue, liver, and immune cells change the composition of plasma, which then reaches other tissues and can alter their gene activity. The study tracked how the two cycling regimes changed the composition of plasma and its effects on fat cells.

The researchers found that 714 out of 2,884 measured proteins changed immediately after sprint cycling, while seven proteins changed immediately after moderate cycling, and 19 changed three hours later. The study also showed that the plasma taken after sprint cycling altered the activity of 1,128 genes and decreased the activity of 549 genes in human fat cells grown in the lab.

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Cell Study Reveals Role


Researchers found that depleting cells of polyamines, molecules that hold reactive iron, led to an increase in labile iron. Cells also became more dependent on GPX4, an enzyme that reduces oxidized membrane fats. Iron is essential for cells, but its reactive part triggers chain reactions that damage membrane fats, leading to ferroptosis.


The team of Ankur Jain conducted a genome-wide CRISPR screen to determine the purpose of the large polyamine reserve. They found that GPX4 was crucial, and its genetic loss or blockade with drugs was fatal to cells with depleted polyamines. Adding spermidine and ferroptosis-inhibiting substances restored cell viability.


The authors linked the polyamine reserve to membrane protection against oxidation. They investigated the cause of GPX4 dependence in iron and found that depleting polyamines increased the level of ferritin, a protein that stores iron. A fluorescent dye showed more reactive iron, and deferroxamine, an iron chelator, restored cell viability when GPX4 was blocked.

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PerturbLDM Model


The PerturbLDM model predicts how drugs change gene activity in cells under unmeasured conditions. A preprint about PerturbLDM was released on August 12 on bioRxiv. It was tested on combinations of drug, dose, and cell line that were hidden during training, but each drug, dose, and line was separately present in the data.


One and the same drug can change gene activity differently in different cell lines - populations of cells that are grown and studied separately. There are so many combinations of drug, dose, and line that laboratories can only measure a part of them. The model is needed to predict in advance which genes will increase or decrease activity in an unmeasured condition. In the preprint, PerturbLDM receives the name of the drug, dose, and cell profile of the same line in a control experiment with DMSO - a solvent that is added instead of the drug.


The model first compresses information about the activity of thousands of genes into a compact record, then gradually builds the response taking into account the drug, dose, and control profile, and then translates it back into gene activities. The authors took 46,471 conditions from Tahoe-100M - a large set of single-cell measurements. For training, they left 32,529, and 13,942 were hidden. Both parts included all 379 drugs, 47 cell lines, and three dose levels. Only a specific triplet was hidden: each of its drug, dose, and cell line was separately familiar to the model.

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Antibody Binding Model


The model, trained on antibody contact regions with targets, more accurately predicted the strength of their binding. On August 13, a study was published in Communications AI & Computing about a language model that reads sequences of both chains of an antibody. The authors hid amino acids during training, primarily in the six CDR loops, where the antibody contacts the target, and tested predictions on variants of antibodies to six antigens.


On a set of 11,052 variants, the prediction quality improved by 26.6% compared to the original model. An antibody recognizes a target with the ends of two protein chains, each with three CDR loops that form the contact surface. The rest of the chain holds the loops in the correct shape, and replacing an amino acid in a loop can change the binding strength.


The language model of proteins learns to restore hidden amino acids in a sequence. During regular training, gaps are randomly distributed throughout the chain, with some tasks falling on framework regions that are relatively similar; CDR loops are more diverse and determine which target the antibody recognizes. The Boston University team trained a model on a pair of heavy and light chains and hid 50% of amino acids within CDR loops.

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Aging Cell Type

Обри де Грей questioned whether one gene shows if a cell retains its type during partial reprogramming. On August 17, Майкл Уэст referenced a graph of two genes during brief induction of Яманаки factors - proteins that change gene function. Обри де Грей responded that an early sign of a cell transitioning to an unspecialized state grows only slightly before TERT, a gene associated with telomerase.


Their exchange raised a practical question: what changes indicate that a cell has altered its age markers but still retains its type. Яманаки factors (OSKM) lead cells to pluripotency when used long-term - a state from which different cell types can arise. With brief OSKM induction, researchers seek a regime in which age markers have shifted, but the cell retains specialization.


In a post on August 17, Уэст wrote that brief OSKM expression may "reverse developmental processes, as in cloning". For clinical application, he terms this approach "induced tissue regeneration" and references a temporal graph from a 2018 study. The graph compares ZFP42 and TERT, with ZFP42 being an early sign of movement towards pluripotency. In a response post, де Грей noted the closeness of these lines: "ZFP42 growth precedes TERT growth by only a little". A short OSKM pulse must be evaluated on a temporal map of several cell programs: age markers, signs of its original type, early and late pluripotency markers, and TERT.

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