Ebola Outbreak
The World Health Organization (WHO) is supporting the PARTNERS trial, which compares treatment options for Bundibugyo virus disease without discontinuing standard medical care. A separate team at the University of Oxford has begun an early trial of a candidate vaccine in volunteers. By August 17, epidemiologist Devi Sridhar wrote in a column for The Guardian that the outbreak in the Democratic Republic of Congo had reached an estimated 4,900 cases and over 2,300 deaths.
The WHO-backed PARTNERS trial randomly assigns patients with confirmed Bundibugyo disease to different antiviral treatment options. In the Democratic Republic of Congo, it is coordinated by the National Institute of Biomedical Research (INRB), a research center of the country's Ministry of Health. All participants receive standard medical care and are monitored for at least 28 days, allowing researchers to compare which treatment regimen is more effective in helping patients survive.
The vaccine is being tested separately: on July 24, the first volunteer at the University of Oxford received the ChAdOx1 BDBV candidate vaccine against Bundibugyo. In the first phase, the team is checking its safety and immune response in volunteers, while the treatment is being studied in patients in the outbreak zone, as reported in The Guardian, August 2023. The possibility of including a patient in the trial depends on how quickly they reach medical help, according to Nature Aging, July 2026.
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The World Health Organization (WHO) is supporting the PARTNERS trial, which compares treatment options for Bundibugyo virus disease without discontinuing standard medical care. A separate team at the University of Oxford has begun an early trial of a candidate vaccine in volunteers. By August 17, epidemiologist Devi Sridhar wrote in a column for The Guardian that the outbreak in the Democratic Republic of Congo had reached an estimated 4,900 cases and over 2,300 deaths.
The WHO-backed PARTNERS trial randomly assigns patients with confirmed Bundibugyo disease to different antiviral treatment options. In the Democratic Republic of Congo, it is coordinated by the National Institute of Biomedical Research (INRB), a research center of the country's Ministry of Health. All participants receive standard medical care and are monitored for at least 28 days, allowing researchers to compare which treatment regimen is more effective in helping patients survive.
The vaccine is being tested separately: on July 24, the first volunteer at the University of Oxford received the ChAdOx1 BDBV candidate vaccine against Bundibugyo. In the first phase, the team is checking its safety and immune response in volunteers, while the treatment is being studied in patients in the outbreak zone, as reported in The Guardian, August 2023. The possibility of including a patient in the trial depends on how quickly they reach medical help, according to Nature Aging, July 2026.
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the Guardian
As Ebola kills thousands in DRC, a perfect storm is making the virus hard to stop | Devi Sridhar
New species and regional instability are factors – but decisions made in the US and Britain are also costing lives, says Devi Sridhar, chair of global public health at the University of Edinburgh
Gromov Hypothesis Solved
The Gromov hypothesis on the growth of space volume has been claimed to be solved in three mathematical manuscripts. Two of these manuscripts reveal the role of AI in the proofs, which were published on arXiv on 13-14 August. In two of the manuscripts, the authors describe the role of generative models in finding the proof.
In 1986, Mikhail Gromov asked if the geometry at each point could limit the growth of an infinite space as a whole. He considered spaces where two mathematical indicators of how space is curved around a point satisfy strict conditions: one is nowhere negative, the other is everywhere positive. For a sphere of radius R in n dimensions, Gromov expected an upper bound of the volume to be C·Rⁿ⁻². Usually, the volume in n dimensions grows like Rⁿ; here the power of the radius is less by two.
The works of Jian Ge, Joacchino Antonelli, and Bochao Kong and Xinyu Zhu all claim this bound. The path from local curvature to volume goes through the spread of heat in space in Ge's work. Antonelli obtains this estimate as a special case of a more general theorem on intermediate curvature. Kong and Zhu relate mass transfer to the volume of spheres of large radius. The three works arrive at the same estimate by different methods.
In two of the manuscripts, the authors separately describe the role of generative models in finding the proofs, citing arXiv and referencing their own work, as well as the assistance of GPT and ChatGPT 5.6 Sol Ultra and Codex in exploring the proof and writing the manuscript.
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The Gromov hypothesis on the growth of space volume has been claimed to be solved in three mathematical manuscripts. Two of these manuscripts reveal the role of AI in the proofs, which were published on arXiv on 13-14 August. In two of the manuscripts, the authors describe the role of generative models in finding the proof.
In 1986, Mikhail Gromov asked if the geometry at each point could limit the growth of an infinite space as a whole. He considered spaces where two mathematical indicators of how space is curved around a point satisfy strict conditions: one is nowhere negative, the other is everywhere positive. For a sphere of radius R in n dimensions, Gromov expected an upper bound of the volume to be C·Rⁿ⁻². Usually, the volume in n dimensions grows like Rⁿ; here the power of the radius is less by two.
The works of Jian Ge, Joacchino Antonelli, and Bochao Kong and Xinyu Zhu all claim this bound. The path from local curvature to volume goes through the spread of heat in space in Ge's work. Antonelli obtains this estimate as a special case of a more general theorem on intermediate curvature. Kong and Zhu relate mass transfer to the volume of spheres of large radius. The three works arrive at the same estimate by different methods.
In two of the manuscripts, the authors separately describe the role of generative models in finding the proofs, citing arXiv and referencing their own work, as well as the assistance of GPT and ChatGPT 5.6 Sol Ultra and Codex in exploring the proof and writing the manuscript.
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Gene Needed for Ear Cell Regeneration
Researchers studied the regeneration of sensory cells in the inner ear of zebrafish larvae. They created a model of inner ear damage and tracked the origin of new hair cells, investigating the role of the dlx5a gene in their regeneration. The vestibular system, which includes hair cells in the inner ear, helps maintain balance by converting head movements into nerve signals.
In the study published in Nature Communications on August 18, the authors introduced the antibiotic neomycin into the inner ear of five-day-old zebrafish larvae, resulting in a 60% reduction of hair cells in the semicircular canals. New cells began to appear within 12 hours, and the vestibulo-ocular reflex returned to control levels within 48 hours.
The authors then tracked the origin of the new cells, labeling supporting cells, which are epithelial cells neighboring hair cells. Some labeled cells acquired hair cell characteristics without visible division, while others divided first. Another label showed that some restored hair cells originated from supporting cells that appeared after the injury, indicating that new hair cells arise through multiple pathways.
To investigate changes in gene function during regeneration, the authors measured gene activity in individual inner ear cells at 6, 24, and 48 hours after damage. They found the most changes in gene activity at 24 hours, with the dlx5a gene, which encodes a protein regulating other genes, being highlighted in supporting cells. The authors used the CRISPR–Cas9 system to disable dlx5a in supporting cells, resulting in poorer hair cell regeneration after injury.
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Researchers studied the regeneration of sensory cells in the inner ear of zebrafish larvae. They created a model of inner ear damage and tracked the origin of new hair cells, investigating the role of the dlx5a gene in their regeneration. The vestibular system, which includes hair cells in the inner ear, helps maintain balance by converting head movements into nerve signals.
In the study published in Nature Communications on August 18, the authors introduced the antibiotic neomycin into the inner ear of five-day-old zebrafish larvae, resulting in a 60% reduction of hair cells in the semicircular canals. New cells began to appear within 12 hours, and the vestibulo-ocular reflex returned to control levels within 48 hours.
The authors then tracked the origin of the new cells, labeling supporting cells, which are epithelial cells neighboring hair cells. Some labeled cells acquired hair cell characteristics without visible division, while others divided first. Another label showed that some restored hair cells originated from supporting cells that appeared after the injury, indicating that new hair cells arise through multiple pathways.
To investigate changes in gene function during regeneration, the authors measured gene activity in individual inner ear cells at 6, 24, and 48 hours after damage. They found the most changes in gene activity at 24 hours, with the dlx5a gene, which encodes a protein regulating other genes, being highlighted in supporting cells. The authors used the CRISPR–Cas9 system to disable dlx5a in supporting cells, resulting in poorer hair cell regeneration after injury.
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Nature
Transcriptomic profiling of inner ear hair cell spontaneous regeneration reveals the key role of dlx5a
Nature Communications - This study establishes a zebrafish inner ear hair cell injury model, characterizes hair cell regeneration at cellular and single-cell transcriptomic levels, and identifies...
FoxM1 Protein Study
Researchers at Kyoto University compared two studies on the FoxM1 protein, which regulates cell division and DNA repair programs. In one study, FoxM1 was briefly activated in young mice, while in the other, it was suppressed in very old mice, removing some senescent cells. The authors linked the difference to age, organ, and cell type.
The review, published on August 17, compared these results, noting that senescent cells stop dividing but remain in tissue, releasing inflammatory signals. FoxM1 may support their survival, and when briefly activated from a young age, tissue restoration programs. In a 2022 study, researchers activated an added active version of FoxM1 in mice from eight weeks of age: three days of work, four days of pause, for a total of 80 weeks.
The authors reported that in progeroid and naturally aging animals, age-related signs weakened, and lifespan increased. In a 2025 article, the authors investigated the link between PGAM1 and Chk1 in senescent cells, finding that their interaction stabilized HIF-2α, a regulator of glucose metabolism genes, and increased FoxM1 activity. The cell received material for nucleotide synthesis, the building blocks of DNA, and maintained a survival program, as described in the Nature Aging, July 2026.
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Researchers at Kyoto University compared two studies on the FoxM1 protein, which regulates cell division and DNA repair programs. In one study, FoxM1 was briefly activated in young mice, while in the other, it was suppressed in very old mice, removing some senescent cells. The authors linked the difference to age, organ, and cell type.
The review, published on August 17, compared these results, noting that senescent cells stop dividing but remain in tissue, releasing inflammatory signals. FoxM1 may support their survival, and when briefly activated from a young age, tissue restoration programs. In a 2022 study, researchers activated an added active version of FoxM1 in mice from eight weeks of age: three days of work, four days of pause, for a total of 80 weeks.
The authors reported that in progeroid and naturally aging animals, age-related signs weakened, and lifespan increased. In a 2025 article, the authors investigated the link between PGAM1 and Chk1 in senescent cells, finding that their interaction stabilized HIF-2α, a regulator of glucose metabolism genes, and increased FoxM1 activity. The cell received material for nucleotide synthesis, the building blocks of DNA, and maintained a survival program, as described in the Nature Aging, July 2026.
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PubMed Central (PMC)
Abrogation of aberrant glycolytic interactions eliminates senescent cells and alleviates aging-related dysfunctions
Cellular senescence is deeply involved in physiological homeostasis, development, tissue repair, aging, and diseases. Senescent cells (SnCs) accumulate in aged tissues and exert deleterious effects by secreting proinflammatory molecules that ...
Anthropic Success
Anthropic designed 1,320 miniproteins for 15 targets, and two laboratories verified their binding on August 18. Anthropic published the campaign results, a full technical report, and open data. Out of 1,320 sequences, 354 were recognized as binding by the combined assessment of two contract laboratories.
The miniprotein in this campaign was required to attach to a selected protein target. To achieve this, a site on the surface of the target needed to be chosen, and the shape and amino acid sequence of the candidate had to be selected, manufactured, and measured for binding. Anthropic selected the targets and prepared a general protocol. Claude studied each target, chose a site on its surface, launched open programs to build the shape and select amino acids, checked candidates on a computer, and selected the final lists for the laboratory.
In Nature Aging, July 2026, similar research was conducted. The current campaign involved a longer chain: the agent itself chose what and how to design, and the laboratory measured each final candidate on a series of targets. In May, Adaptyv Bio tested 100 protein candidates created by ten human teams and six AI agents for TREM2, a protein on immune cells in the brain. In the current campaign, this laboratory participated in verifying 15 targets, and Anthropic revealed the results for each transmitted sequence. Anthropic passed the final sequences to two contract laboratories - Adaptyv Bio and Twist Bioscience.
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Anthropic designed 1,320 miniproteins for 15 targets, and two laboratories verified their binding on August 18. Anthropic published the campaign results, a full technical report, and open data. Out of 1,320 sequences, 354 were recognized as binding by the combined assessment of two contract laboratories.
The miniprotein in this campaign was required to attach to a selected protein target. To achieve this, a site on the surface of the target needed to be chosen, and the shape and amino acid sequence of the candidate had to be selected, manufactured, and measured for binding. Anthropic selected the targets and prepared a general protocol. Claude studied each target, chose a site on its surface, launched open programs to build the shape and select amino acids, checked candidates on a computer, and selected the final lists for the laboratory.
In Nature Aging, July 2026, similar research was conducted. The current campaign involved a longer chain: the agent itself chose what and how to design, and the laboratory measured each final candidate on a series of targets. In May, Adaptyv Bio tested 100 protein candidates created by ten human teams and six AI agents for TREM2, a protein on immune cells in the brain. In the current campaign, this laboratory participated in verifying 15 targets, and Anthropic revealed the results for each transmitted sequence. Anthropic passed the final sequences to two contract laboratories - Adaptyv Bio and Twist Bioscience.
🔗 Read original →
Anthropic
How Claude is accelerating protein design and analytical chemistry
In this post, we share two results that show how Claude can help life scientists increase the pace of their research. In the first, we tested Claude’s ability to design protein binders from scratch, a key step in creating protein-based drugs that has historically…
Aging Cells Impact Therapy
The journal Frontiers in Aging published a review on August 17, 2026, about mesenchymal stromal cells (MSC) and their use in tissue repair and inflammation management. The authors explain that basic quality control may not be enough, as the product may appear viable but perform worse in specific therapies. The review outlines the path of the cell product from donor to patient, including growth, freezing, transportation, and thawing, where cells may experience stress at each stage.
Cell aging is a persistent state where cells divide less often, change their metabolism, and alter the signals they send to surrounding tissue, leading to a decrease in the product's ability to perform its intended function. The authors note that the product may retain acceptable viability and surface markers but have already lost important functionality. The review links stress to loss of function through a chain of events, including DNA damage and mitochondrial dysfunction.
The source of the cells determines where this chain begins, with bone marrow-derived MSC being affected by donor age and inflammation in the bone marrow. Cells from umbilical cord tissue are typically younger but are affected by growth, freezing, thawing, and transportation. For adipose tissue-derived MSC, donor obesity, diabetes, and metabolic inflammation are important factors. The authors suggest linking testing to the product's intended use, such as checking if cells can suppress T-cell activation for inflammation or observing vascular cell migration for tissue repair.
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The journal Frontiers in Aging published a review on August 17, 2026, about mesenchymal stromal cells (MSC) and their use in tissue repair and inflammation management. The authors explain that basic quality control may not be enough, as the product may appear viable but perform worse in specific therapies. The review outlines the path of the cell product from donor to patient, including growth, freezing, transportation, and thawing, where cells may experience stress at each stage.
Cell aging is a persistent state where cells divide less often, change their metabolism, and alter the signals they send to surrounding tissue, leading to a decrease in the product's ability to perform its intended function. The authors note that the product may retain acceptable viability and surface markers but have already lost important functionality. The review links stress to loss of function through a chain of events, including DNA damage and mitochondrial dysfunction.
The source of the cells determines where this chain begins, with bone marrow-derived MSC being affected by donor age and inflammation in the bone marrow. Cells from umbilical cord tissue are typically younger but are affected by growth, freezing, thawing, and transportation. For adipose tissue-derived MSC, donor obesity, diabetes, and metabolic inflammation are important factors. The authors suggest linking testing to the product's intended use, such as checking if cells can suppress T-cell activation for inflammation or observing vascular cell migration for tissue repair.
🔗 Read original →
Frontiers
Frontiers | Mesenchymal stem cell senescence as a potency brake: causes, consequences, and cures
Mesenchymal stem cells (MSCs) are widely investigated for regenerative medicine, tissue repair, immunomodulation, and selected cancer-related applications be...
NeuroQuant PET Approved
The FDA has approved NeuroQuant PET, a program that translates amyloid PET scans into a common scale. On August 12, the FDA granted a "Substantially Equivalent" decision for NeuroQuant PET under the K261916 application. The program automatically generates a quantitative report for amyloid PET scans in patients with cognitive impairments and other neurological conditions.
The amyloid PET scan shows where a tracer accumulates in the brain, binding to amyloid deposits. However, the resulting number depends on the tracer, scan time, device, and calculation method, making it difficult to compare results from different studies and clinics. The Centiloid scale translates these results into common units, with zero corresponding to the average value in young individuals with high confidence in the absence of amyloid, and 100 corresponding to the average value in typical Alzheimer's disease patients.
NeuroQuant PET performs this translation for a given scan, highlighting brain regions, calculating SUVr, and adding the Centiloid value to a structured report. According to Cortechs.ai, the FDA approval applies to amyloid reports for flutemetamol, florbetaben, and florbetapir. The scale, created for research comparison, becomes part of the automatic clinical report, supplementing the image with a number that is equally readable across different tracers and analysis methods.
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The FDA has approved NeuroQuant PET, a program that translates amyloid PET scans into a common scale. On August 12, the FDA granted a "Substantially Equivalent" decision for NeuroQuant PET under the K261916 application. The program automatically generates a quantitative report for amyloid PET scans in patients with cognitive impairments and other neurological conditions.
The amyloid PET scan shows where a tracer accumulates in the brain, binding to amyloid deposits. However, the resulting number depends on the tracer, scan time, device, and calculation method, making it difficult to compare results from different studies and clinics. The Centiloid scale translates these results into common units, with zero corresponding to the average value in young individuals with high confidence in the absence of amyloid, and 100 corresponding to the average value in typical Alzheimer's disease patients.
NeuroQuant PET performs this translation for a given scan, highlighting brain regions, calculating SUVr, and adding the Centiloid value to a structured report. According to Cortechs.ai, the FDA approval applies to amyloid reports for flutemetamol, florbetaben, and florbetapir. The scale, created for research comparison, becomes part of the automatic clinical report, supplementing the image with a number that is equally readable across different tracers and analysis methods.
🔗 Read original →
PR Newswire
Cortechs.ai Announces FDA Clearance for NeuroQuant® PET: Advancing Molecular Imaging for Cognitive Impairment
/PRNewswire/ -- NeuroQuant ® PET has received FDA 510(k) clearance (K261916) for PET. NeuroQuant PET ® aids physicians in the evaluation of patient pathologies...
NeuroQuant PET Approved
The FDA has approved NeuroQuant PET, a program that translates amyloid PET scans into a common scale. On August 12, the FDA granted a "Substantially Equivalent" decision for NeuroQuant PET under the K261916 application. The program automatically generates a quantitative report for amyloid PET scans in patients with cognitive impairments and other neurological conditions.
The amyloid PET scan shows where a tracer accumulates in the brain, binding to amyloid deposits. However, the resulting number depends on the tracer, scan time, device, and calculation method, making it difficult to compare results from different studies and clinics. The Centiloid scale translates these results into common units, with 0 corresponding to the average value in young individuals with high confidence in the absence of amyloid, and 100 corresponding to the average value in typical Alzheimer's disease patients.
NeuroQuant PET performs this translation for a given scan, highlighting brain regions, calculating SUVr, and adding the Centiloid value to a structured report. According to Cortechs.ai, the FDA approval extends to amyloid reports for flutemetamol, florbetaben, and florbetapir. The scale, created for research comparison, becomes part of the automatic clinical report, supplementing the image with a number that is equally readable across different tracers and analysis methods.
🔗 Read original →
The FDA has approved NeuroQuant PET, a program that translates amyloid PET scans into a common scale. On August 12, the FDA granted a "Substantially Equivalent" decision for NeuroQuant PET under the K261916 application. The program automatically generates a quantitative report for amyloid PET scans in patients with cognitive impairments and other neurological conditions.
The amyloid PET scan shows where a tracer accumulates in the brain, binding to amyloid deposits. However, the resulting number depends on the tracer, scan time, device, and calculation method, making it difficult to compare results from different studies and clinics. The Centiloid scale translates these results into common units, with 0 corresponding to the average value in young individuals with high confidence in the absence of amyloid, and 100 corresponding to the average value in typical Alzheimer's disease patients.
NeuroQuant PET performs this translation for a given scan, highlighting brain regions, calculating SUVr, and adding the Centiloid value to a structured report. According to Cortechs.ai, the FDA approval extends to amyloid reports for flutemetamol, florbetaben, and florbetapir. The scale, created for research comparison, becomes part of the automatic clinical report, supplementing the image with a number that is equally readable across different tracers and analysis methods.
🔗 Read original →
PR Newswire
Cortechs.ai Announces FDA Clearance for NeuroQuant® PET: Advancing Molecular Imaging for Cognitive Impairment
/PRNewswire/ -- NeuroQuant ® PET has received FDA 510(k) clearance (K261916) for PET. NeuroQuant PET ® aids physicians in the evaluation of patient pathologies...
Brain Atlas Study
A recent study published in Cell on August 18 has created a detailed map of the brain of 23 female macaques, highlighting the white matter of the brain stem as particularly vulnerable to age-related changes. The researchers collected 2,955,873 cell nuclei and tracked how age-related shifts are distributed across different brain regions and cell types.
The study found that the brain ages unevenly in different regions and cells, with the most consistent age-related shifts found in the pons and medulla - regions of the brain stem. The white matter in these regions consists of bundles of nerve fibers coated with myelin, a fatty substance that accelerates signal transmission. The researchers observed a decline in the activity of genes related to myelin and lipid synthesis in oligodendrocytes, the cells responsible for producing myelin.
The study's findings also showed changes in the signals of cells that support nerve tissue or give rise to oligodendrocytes. The researchers confirmed a decrease in PDGFRA gene RNA in oligodendrocyte precursor cells, which codes for a receptor of growth signals. The study's data is available on the NHPABC portal, allowing researchers to search for age-related shifts by specific brain region, cell type, and programs related to myelin.
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A recent study published in Cell on August 18 has created a detailed map of the brain of 23 female macaques, highlighting the white matter of the brain stem as particularly vulnerable to age-related changes. The researchers collected 2,955,873 cell nuclei and tracked how age-related shifts are distributed across different brain regions and cell types.
The study found that the brain ages unevenly in different regions and cells, with the most consistent age-related shifts found in the pons and medulla - regions of the brain stem. The white matter in these regions consists of bundles of nerve fibers coated with myelin, a fatty substance that accelerates signal transmission. The researchers observed a decline in the activity of genes related to myelin and lipid synthesis in oligodendrocytes, the cells responsible for producing myelin.
The study's findings also showed changes in the signals of cells that support nerve tissue or give rise to oligodendrocytes. The researchers confirmed a decrease in PDGFRA gene RNA in oligodendrocyte precursor cells, which codes for a receptor of growth signals. The study's data is available on the NHPABC portal, allowing researchers to search for age-related shifts by specific brain region, cell type, and programs related to myelin.
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Virtual Cell Technology
GenBio AI has introduced a digital cell system, AIDO Cell, which allows biologists to experiment on a computer. AIDO Cell is a "virtual cell" that belongs to a new generation of AI models attempting to model entire biological systems, rather than just predicting individual properties. The main difference from systems like AlphaFold is the scale, as AlphaFold can predict protein structure from amino acid sequences, but a protein is just one element of a cell.
AIDO attempts to link multiple levels of biology: DNA → RNA → proteins → cellular processes → overall cell behavior. The ability to conduct virtual experiments is particularly interesting, as researchers can set up an experiment, such as changing the activity of a specific gene or adding a drug, and the model attempts to predict the consequences at different levels of biology.
The system retains the state of the system between experiments, allowing for more complex and realistic simulations. For example, if a researcher first changes one gene and then adds a drug, the second experiment can take into account the consequences of the first. This is a significant departure from traditional prediction models, where each prediction is treated as an independent question. As demonstrated by GenBio using imatinib, a drug used to treat certain types of leukemia, the model was able to reproduce the known mechanism of action at multiple levels of cellular biology, as reported in Nature Aging, July 2026.
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GenBio AI has introduced a digital cell system, AIDO Cell, which allows biologists to experiment on a computer. AIDO Cell is a "virtual cell" that belongs to a new generation of AI models attempting to model entire biological systems, rather than just predicting individual properties. The main difference from systems like AlphaFold is the scale, as AlphaFold can predict protein structure from amino acid sequences, but a protein is just one element of a cell.
AIDO attempts to link multiple levels of biology: DNA → RNA → proteins → cellular processes → overall cell behavior. The ability to conduct virtual experiments is particularly interesting, as researchers can set up an experiment, such as changing the activity of a specific gene or adding a drug, and the model attempts to predict the consequences at different levels of biology.
The system retains the state of the system between experiments, allowing for more complex and realistic simulations. For example, if a researcher first changes one gene and then adds a drug, the second experiment can take into account the consequences of the first. This is a significant departure from traditional prediction models, where each prediction is treated as an independent question. As demonstrated by GenBio using imatinib, a drug used to treat certain types of leukemia, the model was able to reproduce the known mechanism of action at multiple levels of cellular biology, as reported in Nature Aging, July 2026.
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Nature
How to build an AI-driven digital organism
Nature Medicine - Manipulating biology in the physical world is complex; the authors envision an AI-driven digital organism—a system of integrated multiscale foundation models—detailing...
Gene editing boost
The University of Wisconsin-Madison team published a genetic screen on August 13, in which they sequentially turned off 19,114 human genes and observed how it changed the work of the DNA editor, delivered by lipid nanoparticles. Six genes passed the re-test, and the shutdown of GJB2 and BET1L enhanced editing in several cellular models.
The DNA editor Cas9 was delivered in a lipid nanoparticle - a fatty shell with protein and guide RNA. After entering the cell, the cargo must be released from the intracellular bubble and reach the nucleus, where the DNA is located. In this screen, one gene was turned off in each cell, and sequencing - reading the DNA sequence - showed which gene was turned off and whether the editor was able to change the desired site.
The authors separately checked 26 candidates, and six had a repeated effect. The shutdown of GJB2 and BET1L increased the efficiency of editors that change individual "letters" of DNA without cutting both strands. In cells with a model mutation KCNJ13, the suppression of GJB2 gave 19.3% corrections - 6.7 times more than in control cells.
The team then checked at what point in the path the difference arises, as described in the Nature Aging, July 2026 journal. When Cas9 was introduced by electroporation - an electric pulse through the cell membrane - the advantage of cells with turned-off genes disappeared in most candidate lines.
🔗 Read original →
The University of Wisconsin-Madison team published a genetic screen on August 13, in which they sequentially turned off 19,114 human genes and observed how it changed the work of the DNA editor, delivered by lipid nanoparticles. Six genes passed the re-test, and the shutdown of GJB2 and BET1L enhanced editing in several cellular models.
The DNA editor Cas9 was delivered in a lipid nanoparticle - a fatty shell with protein and guide RNA. After entering the cell, the cargo must be released from the intracellular bubble and reach the nucleus, where the DNA is located. In this screen, one gene was turned off in each cell, and sequencing - reading the DNA sequence - showed which gene was turned off and whether the editor was able to change the desired site.
The authors separately checked 26 candidates, and six had a repeated effect. The shutdown of GJB2 and BET1L increased the efficiency of editors that change individual "letters" of DNA without cutting both strands. In cells with a model mutation KCNJ13, the suppression of GJB2 gave 19.3% corrections - 6.7 times more than in control cells.
The team then checked at what point in the path the difference arises, as described in the Nature Aging, July 2026 journal. When Cas9 was introduced by electroporation - an electric pulse through the cell membrane - the advantage of cells with turned-off genes disappeared in most candidate lines.
🔗 Read original →
PubMed Central (PMC)
Genome-wide CRISPR screening identifies cellular factors controlling nonviral genome editing efficiency
To systematically map cellular factors constraining nonviral genome editing, influencing uptake and intracellular trafficking, we develop a genome-wide CRISPR screening platform linking perturbation of 19,114 genes to editing outcomes in human ...
Bone Tissue Restored
Researchers have partially restored the mineral and mechanical signals of aging bone tissue using OsteoVes, artificial particles designed to restore mineral deposition and mechanical signals in aging bone tissue. In experiments with cells from elderly donors, old mice, and three macaques, they shifted measurable indicators towards bone formation.
The study, published in Cell Reports Medicine on August 18, found that mesenchymal stromal cells in bone marrow can become either bone-building cells or fat cells, influenced by the extracellular matrix, a environment of proteins and minerals surrounding the cell. With age, the matrix becomes less effective at depositing minerals and transmitting mechanical signals to cells.
The authors of the new study had previously altered the mechanical properties of the environment in bone injuries using a hydrogel that mimicked a blood clot, helping cells to activate their bone formation program. Now, they have tested whether temporarily replacing the functions of the matrix can direct bone marrow cells towards bone formation, even in aging tissue. The OsteoVes particles, which mimic matrix vesicles of bone tissue, contain alkaline phosphatase that breaks down pyrophosphate, which hinders mineralization, and hydroxyapatite nanoparticles, which provide a starting point for mineral deposition.
The authors compared the complete construct to its individual components and found that OsteoVes enhanced the formation of mineralized matrix and the activity of genes associated with bone formation in old human stromal cells. Variants without the enzyme or hydroxyapatite and empty membrane vesicles were less effective. When the researchers blocked PIEZO1, a protein channel that helps cells respond to mechanical stimuli, the effect was also weakened. The authors then tested whether the bone tissue of old animals could be changed, and found that two intravenous doses of OsteoVes administered one week apart increased the maximum load that the femur could withstand by approximately 1.4 times in 22-month-old mice, and improved the bending strength by approximately 95% compared to a saline control.
🔗 Read original →
Researchers have partially restored the mineral and mechanical signals of aging bone tissue using OsteoVes, artificial particles designed to restore mineral deposition and mechanical signals in aging bone tissue. In experiments with cells from elderly donors, old mice, and three macaques, they shifted measurable indicators towards bone formation.
The study, published in Cell Reports Medicine on August 18, found that mesenchymal stromal cells in bone marrow can become either bone-building cells or fat cells, influenced by the extracellular matrix, a environment of proteins and minerals surrounding the cell. With age, the matrix becomes less effective at depositing minerals and transmitting mechanical signals to cells.
The authors of the new study had previously altered the mechanical properties of the environment in bone injuries using a hydrogel that mimicked a blood clot, helping cells to activate their bone formation program. Now, they have tested whether temporarily replacing the functions of the matrix can direct bone marrow cells towards bone formation, even in aging tissue. The OsteoVes particles, which mimic matrix vesicles of bone tissue, contain alkaline phosphatase that breaks down pyrophosphate, which hinders mineralization, and hydroxyapatite nanoparticles, which provide a starting point for mineral deposition.
The authors compared the complete construct to its individual components and found that OsteoVes enhanced the formation of mineralized matrix and the activity of genes associated with bone formation in old human stromal cells. Variants without the enzyme or hydroxyapatite and empty membrane vesicles were less effective. When the researchers blocked PIEZO1, a protein channel that helps cells respond to mechanical stimuli, the effect was also weakened. The authors then tested whether the bone tissue of old animals could be changed, and found that two intravenous doses of OsteoVes administered one week apart increased the maximum load that the femur could withstand by approximately 1.4 times in 22-month-old mice, and improved the bending strength by approximately 95% compared to a saline control.
🔗 Read original →
Cell Reports Medicine
Functional matrix vesicle replacement partially restores chemo-mechanical coupling in the aged bone niche
Zhang et al. develop OsteoVes, a matrix-vesicle-mimetic replacement that restores
Pi/PPi balance, ECM anchoring, and mechanotransduction in aged bone niches. OsteoVes
rescues osteogenic defects in elderly patient-derived MSCs and improves short-term
bone…
Pi/PPi balance, ECM anchoring, and mechanotransduction in aged bone niches. OsteoVes
rescues osteogenic defects in elderly patient-derived MSCs and improves short-term
bone…
Brain Cell Aging
Researchers studied how different brain cell types interact and transmit signs of aging. On August 15, a study was published in Aging Cell, where scientists transferred media from five human brain cell types to each other and measured which cells developed signs of aging. A 15-day experiment showed that astrocytes and microglia more often triggered such responses in other cells.
The study focused on cellular aging, or senescence, a state where a cell stops dividing and changes its function after stress. It releases a set of proteins and molecules, known as SASP, into the surrounding environment, which can alter the state of neighboring cells. The authors worked with five human immortalized cell lines, including astrocytes, vascular lining cells, microglia, oligodendrocytes, and neuron-like cells.
The cell cultures were treated with BrdU for seven days to induce signs of aging. Then, the media from each cell type was transferred to other cells. The media from treated astrocytes and microglia increased the proportion of cells with SA-β-gal, a senescence marker, in astrocytes and vascular lining cells. Microglia responded to media from several other cell types, and the authors further checked other senescence markers, such as DNA damage and mitochondrial function.
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Researchers studied how different brain cell types interact and transmit signs of aging. On August 15, a study was published in Aging Cell, where scientists transferred media from five human brain cell types to each other and measured which cells developed signs of aging. A 15-day experiment showed that astrocytes and microglia more often triggered such responses in other cells.
The study focused on cellular aging, or senescence, a state where a cell stops dividing and changes its function after stress. It releases a set of proteins and molecules, known as SASP, into the surrounding environment, which can alter the state of neighboring cells. The authors worked with five human immortalized cell lines, including astrocytes, vascular lining cells, microglia, oligodendrocytes, and neuron-like cells.
The cell cultures were treated with BrdU for seven days to induce signs of aging. Then, the media from each cell type was transferred to other cells. The media from treated astrocytes and microglia increased the proportion of cells with SA-β-gal, a senescence marker, in astrocytes and vascular lining cells. Microglia responded to media from several other cell types, and the authors further checked other senescence markers, such as DNA damage and mitochondrial function.
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PubMed Central (PMC)
Characterizing the SASP‐Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types
One of the defining phenotypes of a senescent cell is the senescence‐associated secretory phenotype (SASP), which can propagate senescence in neighboring cells both in vitro and in vivo. Importantly, this paracrine spreading of senescence can act in ...
AIntibody Test Results
The AIntibody blind test involved 511 antibodies submitted by 29 organizations for three tasks, with independent laboratories synthesizing and testing them under the same conditions. An antibody is a protein that recognizes and binds to a specific target, requiring a strong bond, sufficient production, stable form, and selectivity to its target.
The competition measured both the rare best result and the fraction of variants that a laboratory could work with further, using the logic of blind tests from CASP. The AIntibody competition continued from 2024, where participants submitted antibody sequences in advance, with all variants first tested using surface plasmon resonance to measure binding to the target, and the strongest further measured using KinExA.
In the task of improving an already known antibody, a variant from company Aureka bound to the target as strongly as the best laboratory variant, with 94.7 versus 113 pM by KinExA, and their 95% uncertainty intervals overlapped. This was the result of one team in the task where participants were given data from the first stage of laboratory selection, with the target being the RBD of SARS-CoV-2. The results were published in Nature Biotechnology on August 19.
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The AIntibody blind test involved 511 antibodies submitted by 29 organizations for three tasks, with independent laboratories synthesizing and testing them under the same conditions. An antibody is a protein that recognizes and binds to a specific target, requiring a strong bond, sufficient production, stable form, and selectivity to its target.
The competition measured both the rare best result and the fraction of variants that a laboratory could work with further, using the logic of blind tests from CASP. The AIntibody competition continued from 2024, where participants submitted antibody sequences in advance, with all variants first tested using surface plasmon resonance to measure binding to the target, and the strongest further measured using KinExA.
In the task of improving an already known antibody, a variant from company Aureka bound to the target as strongly as the best laboratory variant, with 94.7 versus 113 pM by KinExA, and their 95% uncertainty intervals overlapped. This was the result of one team in the task where participants were given data from the first stage of laboratory selection, with the target being the RBD of SARS-CoV-2. The results were published in Nature Biotechnology on August 19.
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Nature
A blinded, prospective benchmark of in silico antibody discovery anchored to experimental affinity and developability
Nature Biotechnology - A prospective, blinded competition is conducted for artificial-intelligence-generated and optimized antibody discovery.
Ben Goertzel's Omega Point
Ben Goertzel published an essay "Arrow of Time, Part 2" on August 15, where he links subjective time to the recording of new significant differences and suggests leaving a history of changes for future mind versions. As the mind rewrites models, expands memory, and learns to reason anew, its future version stores and processes experience differently. The connection between versions is maintained by whether a later version can translate previous ways of representing experience into its new representations.
The analysis of digital personality continuity separates working memory, holding current thought, from episodic memory, which links a person to the past. Goertzel sets a related technical challenge for the self-modifying mind: a later version needs an archive that it can read after changing its own ways of thinking. In Goertzel's model, subjective time grows with the record of significant differences: they change the world model and help choose actions later. When the system masters unfamiliar situations, it must preserve the differences on which choice depends.
Goertzel comes to the "Omega Point": the mind retains a common direction - values, ability to correct itself, and coordinate its parts - as the history of experience continues to grow. In this model, stability lies in the direction, while the internal state changes with the growing history. Rapid self-modification increases the requirement for such continuity. Goertzel formulates it as: "The faster the stream of differences, the smaller the average self-translation error should become." As an engineering step, he suggests dividing memory into two parts: working memory that can be rewritten and a replenished journal where the system's conclusions are recorded. This journal retains both corrections and deletions; a later version can compare its transformations with how early representations were organized. Goertzel's philosophical question about personality continuity takes on an engineering form: a future version of the mind must be able to read its own history and verify the connection with early representations, as discussed in Nature Aging, July 2026.
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Ben Goertzel published an essay "Arrow of Time, Part 2" on August 15, where he links subjective time to the recording of new significant differences and suggests leaving a history of changes for future mind versions. As the mind rewrites models, expands memory, and learns to reason anew, its future version stores and processes experience differently. The connection between versions is maintained by whether a later version can translate previous ways of representing experience into its new representations.
The analysis of digital personality continuity separates working memory, holding current thought, from episodic memory, which links a person to the past. Goertzel sets a related technical challenge for the self-modifying mind: a later version needs an archive that it can read after changing its own ways of thinking. In Goertzel's model, subjective time grows with the record of significant differences: they change the world model and help choose actions later. When the system masters unfamiliar situations, it must preserve the differences on which choice depends.
Goertzel comes to the "Omega Point": the mind retains a common direction - values, ability to correct itself, and coordinate its parts - as the history of experience continues to grow. In this model, stability lies in the direction, while the internal state changes with the growing history. Rapid self-modification increases the requirement for such continuity. Goertzel formulates it as: "The faster the stream of differences, the smaller the average self-translation error should become." As an engineering step, he suggests dividing memory into two parts: working memory that can be rewritten and a replenished journal where the system's conclusions are recorded. This journal retains both corrections and deletions; a later version can compare its transformations with how early representations were organized. Goertzel's philosophical question about personality continuity takes on an engineering form: a future version of the mind must be able to read its own history and verify the connection with early representations, as discussed in Nature Aging, July 2026.
🔗 Read original →
Substack
Time’s Arrow, Part 2: Relating Subjective Time-Flow to Intelligence and Consciousness Expansion
Why intelligence-in-action may require a minimum flow of meaningful distinctions, why enlightenment may involve more meta-distinction rather than fewer distinctions, and why an Omega mind should be an expanding ray rather than a frozen point
Stroke Recovery Boost
The IpsiHand home system, which reads brain electrical signals, improved hand movement after stroke more than exercises. On August 13, a randomized BCI-REHAB study was published, with a primary analysis of 62 people with chronic hand movement impairment after stroke. It compared the IpsiHand home neurointerface with exercises.
The system converts an attempt to move the affected hand into finger movement; the control group trained their hand on the same schedule. For some people after stroke, attempting to move their hand no longer leads to wrist movement. IpsiHand builds rehabilitation around this attempt: EEG - recording electrical brain activity from the surface of the head - captures a signal pattern in the unaffected hemisphere associated with imagined movement of the affected hand.
When the system recognizes it, a device attached to the wrist opens and closes the fingers in a three-finger grip. Early research showed that such a signal can be used to control wrist movement. The BCI-REHAB study checked if this connection improves rehabilitation more than the same amount of home exercises. Before distribution, each participant's EEG signal was checked to see if it was sufficient to control the device. The primary analysis included 37 people with IpsiHand and 25 with a hand, wrist, elbow, and shoulder movement program, including household tasks: opening a drawer or lifting a cup.
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The IpsiHand home system, which reads brain electrical signals, improved hand movement after stroke more than exercises. On August 13, a randomized BCI-REHAB study was published, with a primary analysis of 62 people with chronic hand movement impairment after stroke. It compared the IpsiHand home neurointerface with exercises.
The system converts an attempt to move the affected hand into finger movement; the control group trained their hand on the same schedule. For some people after stroke, attempting to move their hand no longer leads to wrist movement. IpsiHand builds rehabilitation around this attempt: EEG - recording electrical brain activity from the surface of the head - captures a signal pattern in the unaffected hemisphere associated with imagined movement of the affected hand.
When the system recognizes it, a device attached to the wrist opens and closes the fingers in a three-finger grip. Early research showed that such a signal can be used to control wrist movement. The BCI-REHAB study checked if this connection improves rehabilitation more than the same amount of home exercises. Before distribution, each participant's EEG signal was checked to see if it was sufficient to control the device. The primary analysis included 37 people with IpsiHand and 25 with a hand, wrist, elbow, and shoulder movement program, including household tasks: opening a drawer or lifting a cup.
🔗 Read original →
PubMed Central (PMC)
IpsiHand Brain–Computer Interface Therapy Induces Broad Upper Extremity Motor Rehabilitation in Chronic Stroke
Chronic hemiparetic stroke patients have very limited benefits from current therapies. Brain–computer interface (BCI) engaging the unaffected hemisphere has emerged as a promising novel therapeutic approach for chronic stroke rehabilitation. This ...
Aging Skin Study
Researchers found that in the aging epidermis of mice, the proteins BMAL1 and YAP together activate inflammatory genes. A recent study published in Nature Aging, August 2026 investigated the outer layer of mouse skin, tracing how BMAL1, a biological clock protein, and YAP, a protein responding to tissue mechanical properties, alter the function of inflammation genes.
The epidermal cells of old mice receive two changing signals: one from the tissue beneath them and another from immune cells. The basement membrane, a thin layer between the epidermis and the deeper dermis, resists deformation more strongly, while the dermis accumulates cells releasing IL-17, a molecule signaling inflammation.
The authors compared adult and old epidermis at six points in the daily cycle, finding that among 118 inflammatory genes more active in old skin, only four changed rhythmically. This suggests that BMAL1 is involved in a sustained age-related reorganization of gene function, not just daily fluctuations.
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Researchers found that in the aging epidermis of mice, the proteins BMAL1 and YAP together activate inflammatory genes. A recent study published in Nature Aging, August 2026 investigated the outer layer of mouse skin, tracing how BMAL1, a biological clock protein, and YAP, a protein responding to tissue mechanical properties, alter the function of inflammation genes.
The epidermal cells of old mice receive two changing signals: one from the tissue beneath them and another from immune cells. The basement membrane, a thin layer between the epidermis and the deeper dermis, resists deformation more strongly, while the dermis accumulates cells releasing IL-17, a molecule signaling inflammation.
The authors compared adult and old epidermis at six points in the daily cycle, finding that among 118 inflammatory genes more active in old skin, only four changed rhythmically. This suggests that BMAL1 is involved in a sustained age-related reorganization of gene function, not just daily fluctuations.
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Nature
Noncircadian BMAL1–YAP activity amplifies persistent inflammation in aged epidermis
Nature Aging - Chronic inflammation is a hallmark of aging, yet the underlying molecular mechanisms are incompletely understood. Here the authors show that, in the skin, BMAL1 and YAP cooperate at...
US Seeks Bio Risk Protection
The US White House is seeking protection from biological risks associated with AI after cutting a high-profile team. By the end of the Joe Biden administration, the White House had up to 30 biodefense specialists. After cuts and reorganizations, former officials said there were periods when no dedicated staff member was working on the issue. Protection from biological risks of AI involves several actions, including assessing risk throughout the workflow of a trained biologist.
The risk assessment path shows that a model can help design a DNA sequence, a synthetic DNA supplier can check an order, and a laboratory can provide access to equipment and biological samples. Government policy connects these points with rules and agency work. One of these points is the ordering of synthetic DNA. The 2024 framework tied federal funding to sequence and buyer screening: laboratories must purchase DNA, other nucleic acids, and desktop devices for their synthesis from suppliers that comply with these requirements.
A White House directive on May 5, 2025, gave the White House Office of Science and Technology Policy 90 days to review or replace the framework. On July 28, the US Department of Health and Human Services announced a new national policy for oversight of high-risk life sciences research, which prohibits federal funding for certain work that intentionally enhances dangerous properties of pathogens and introduces independent review of certain high-risk research, as reported in The Washington Post.
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The US White House is seeking protection from biological risks associated with AI after cutting a high-profile team. By the end of the Joe Biden administration, the White House had up to 30 biodefense specialists. After cuts and reorganizations, former officials said there were periods when no dedicated staff member was working on the issue. Protection from biological risks of AI involves several actions, including assessing risk throughout the workflow of a trained biologist.
The risk assessment path shows that a model can help design a DNA sequence, a synthetic DNA supplier can check an order, and a laboratory can provide access to equipment and biological samples. Government policy connects these points with rules and agency work. One of these points is the ordering of synthetic DNA. The 2024 framework tied federal funding to sequence and buyer screening: laboratories must purchase DNA, other nucleic acids, and desktop devices for their synthesis from suppliers that comply with these requirements.
A White House directive on May 5, 2025, gave the White House Office of Science and Technology Policy 90 days to review or replace the framework. On July 28, the US Department of Health and Human Services announced a new national policy for oversight of high-risk life sciences research, which prohibits federal funding for certain work that intentionally enhances dangerous properties of pathogens and introduces independent review of certain high-risk research, as reported in The Washington Post.
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Bone Repair Falters
After repeated injury in mice, less new bone formed, although the bone marrow appeared recovered. In an article published on August 19 in Nature Communications, scientists investigated whether bone marrow cells could re-engage in bone repair after a previous injury. After a second injury, their descendants less often became osteoblasts, and less new bone formed.
The bone marrow's stromal cells support the environment within the bone marrow. After injury, some of these cells can become osteoblasts - cells that build bone. To track this change, the authors genetically labeled cells in mice and compared one and two operations that triggered bone marrow repair. After the second operation, micro-CT scans showed that less new trabecular bone formed.
The labeled cells less often transformed into osteoblasts, and their descendants more often became adipocytes of the bone marrow. In a separate model of repeated fractures, the same pattern emerged: less new bone and osteoblasts, more adipocyte descendants. Initially, the interval between operations was about four weeks. By the next injury, the bone marrow under the microscope already appeared comparable to the undamaged one.
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After repeated injury in mice, less new bone formed, although the bone marrow appeared recovered. In an article published on August 19 in Nature Communications, scientists investigated whether bone marrow cells could re-engage in bone repair after a previous injury. After a second injury, their descendants less often became osteoblasts, and less new bone formed.
The bone marrow's stromal cells support the environment within the bone marrow. After injury, some of these cells can become osteoblasts - cells that build bone. To track this change, the authors genetically labeled cells in mice and compared one and two operations that triggered bone marrow repair. After the second operation, micro-CT scans showed that less new trabecular bone formed.
The labeled cells less often transformed into osteoblasts, and their descendants more often became adipocytes of the bone marrow. In a separate model of repeated fractures, the same pattern emerged: less new bone and osteoblasts, more adipocyte descendants. Initially, the interval between operations was about four weeks. By the next injury, the bone marrow under the microscope already appeared comparable to the undamaged one.
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Nature
Injury-driven stromal exhaustion disrupts intrinsic regenerative capability
Nature Communications - This study reveals a finite regenerative capacity of Lepr+Cxcl12+ stromal cells, showing that repeated injury drives stromal exhaustion, adipogenic lineage switching, and...
Brain Blood Flow
The protein cMAF helps immune cells near brain artery walls maintain vessel response to CO2 and cerebrospinal fluid movement. On August 14, authors described this mechanism, finding that perivascular macrophages depend on cMAF to function properly.
When cMAF was removed in mice, cerebrospinal fluid movement and vessel response to excess CO2 were disrupted. Researchers had previously shown in 2022 that perivascular macrophages participate in cerebrospinal fluid movement, and now sought to understand the genetic program supporting these cells' function.
Authors compared gene activity in different brain macrophages and identified cMAF. They then removed the Maf gene, which codes for cMAF, in mice, finding that macrophages around arteries lost a characteristic set of active genes, and fluorescent marker flow decreased along the middle cerebral artery.
The authors investigated how this relates to vessel function, administering a mixture with 10% CO2 to mice. In control animals, arteries dilated and brain blood flow increased, but this response disappeared after cMAF removal. The protein IGF1 was found to be a key signal transmitted from macrophages to the vessel wall, with IGF1R as its receptor.
In human brain data, MAF was found to be the most active regulator in perivascular macrophages, with its activity and IGF1 levels increasing with amyloid deposits in APOE3 variant carriers. A genetic variant near MAF was associated with higher MAF activity and lower Alzheimer's disease risk, as described in Nature Aging, July 2026.
🔗 Read original →
The protein cMAF helps immune cells near brain artery walls maintain vessel response to CO2 and cerebrospinal fluid movement. On August 14, authors described this mechanism, finding that perivascular macrophages depend on cMAF to function properly.
When cMAF was removed in mice, cerebrospinal fluid movement and vessel response to excess CO2 were disrupted. Researchers had previously shown in 2022 that perivascular macrophages participate in cerebrospinal fluid movement, and now sought to understand the genetic program supporting these cells' function.
Authors compared gene activity in different brain macrophages and identified cMAF. They then removed the Maf gene, which codes for cMAF, in mice, finding that macrophages around arteries lost a characteristic set of active genes, and fluorescent marker flow decreased along the middle cerebral artery.
The authors investigated how this relates to vessel function, administering a mixture with 10% CO2 to mice. In control animals, arteries dilated and brain blood flow increased, but this response disappeared after cMAF removal. The protein IGF1 was found to be a key signal transmitted from macrophages to the vessel wall, with IGF1R as its receptor.
In human brain data, MAF was found to be the most active regulator in perivascular macrophages, with its activity and IGF1 levels increasing with amyloid deposits in APOE3 variant carriers. A genetic variant near MAF was associated with higher MAF activity and lower Alzheimer's disease risk, as described in Nature Aging, July 2026.
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Cell
Brain perivascular macrophages regulate endothelial cell function via a cMAF-dependent transcriptional program in mouse and human
This study identifies cMAF as a key transcription factor that orchestrates the molecular
crosstalk between brain perivascular macrophages and arteries, thereby sustaining
cerebrovascular function in health and disease.
crosstalk between brain perivascular macrophages and arteries, thereby sustaining
cerebrovascular function in health and disease.
Brain Organoids Live
Brain organoids, once limited to a few months of life, can now survive for years and age like real brains. These tiny tissue pieces, created from stem cells, mimic the earliest stages of human brain development. Typically, such organoids are grown for 2-3 months, but a new study has kept them alive for up to seven years. This allowed researchers to observe how brain cells change over long periods: which cell types emerge, how their function changes, and how gene activity shifts. Most interestingly, they began to show signs of "aging" as metabolic groups accumulated in their DNA.
The lab-grown tissue did not just exist for a long time; it underwent similar maturation and aging processes as a real brain. Researchers observed a diversity of cells, the formation of more complex structures, and changes that usually occur in the human brain over many years. This is particularly useful, given that some diseases (Parkinson's, schizophrenia, Alzheimer's) only manifest with age. Previously, it was impossible to study these diseases using organoids, as the model did not survive long enough to reach the necessary stage. Now, scientists have a tool to observe long-term changes in neural networks and cellular processes, as reported in Nature, July 2026.
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Brain organoids, once limited to a few months of life, can now survive for years and age like real brains. These tiny tissue pieces, created from stem cells, mimic the earliest stages of human brain development. Typically, such organoids are grown for 2-3 months, but a new study has kept them alive for up to seven years. This allowed researchers to observe how brain cells change over long periods: which cell types emerge, how their function changes, and how gene activity shifts. Most interestingly, they began to show signs of "aging" as metabolic groups accumulated in their DNA.
The lab-grown tissue did not just exist for a long time; it underwent similar maturation and aging processes as a real brain. Researchers observed a diversity of cells, the formation of more complex structures, and changes that usually occur in the human brain over many years. This is particularly useful, given that some diseases (Parkinson's, schizophrenia, Alzheimer's) only manifest with age. Previously, it was impossible to study these diseases using organoids, as the model did not survive long enough to reach the necessary stage. Now, scientists have a tool to observe long-term changes in neural networks and cellular processes, as reported in Nature, July 2026.
🔗 Read original →
Nature
Human brain organoids record the passage of time over multiple years
Nature - Human brain organoids were developed for over five years in culture to demonstrate that brain cells can continue to mature and record the passage of time, following human-specific...