Longevity Leaders
TIME magazine has released a collection of 12 profiles on aging biology, from cell reprogramming to human trials. The Longevity Leaders 2026 issue features individuals working to change, measure, and test age-related processes in cells and humans. The discovery by Sinyi Yamanaka led to cell reprogramming attempts to restore cells to a younger state.
The magazine includes David Sinclair and Juan Carlos Izpisua Belmonte, who are developing this research line. Nir Barzilai studies the genetic and biological characteristics of people who remain healthy after 95 years and is involved in the search for biomarkers - measurable signs of age-related changes.
Andrea Maier takes this question to human trials, often recruiting participants with a higher biological age than their calendar age. Steve Horvath's work helps select the group, and a planned randomized trial will test whether the intervention helps this group. The XPRIZE Healthspan competition adds a general way to compare different approaches, with finalists evaluating the effects of interventions on muscle, cognitive, and immune function, as cited in Nature Aging, July 2026.
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TIME magazine has released a collection of 12 profiles on aging biology, from cell reprogramming to human trials. The Longevity Leaders 2026 issue features individuals working to change, measure, and test age-related processes in cells and humans. The discovery by Sinyi Yamanaka led to cell reprogramming attempts to restore cells to a younger state.
The magazine includes David Sinclair and Juan Carlos Izpisua Belmonte, who are developing this research line. Nir Barzilai studies the genetic and biological characteristics of people who remain healthy after 95 years and is involved in the search for biomarkers - measurable signs of age-related changes.
Andrea Maier takes this question to human trials, often recruiting participants with a higher biological age than their calendar age. Steve Horvath's work helps select the group, and a planned randomized trial will test whether the intervention helps this group. The XPRIZE Healthspan competition adds a general way to compare different approaches, with finalists evaluating the effects of interventions on muscle, cognitive, and immune function, as cited in Nature Aging, July 2026.
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Nature
Anti-aging interventions need less hype and more clinical evidence
Nature Medicine - The aging field needs to develop reliable biomarkers of aging and a solid evidence base for the safety and efficacy of anti-aging treatments.
Telomere Protein Found
Researchers have discovered the telomere protein TRF2 on DNA fragments associated with inflammation in cells that have stopped dividing. In several models of human cells, scientists observed DNA fragments with TRF2 - a protein that protects telomeres, the ends of chromosomes - in the cytoplasm. These fragments showed signs of DNA damage and cGAS, a protein that recognizes DNA in the cytoplasm.
The nucleus normally keeps chromosomes inside the cell. When DNA enters the cytoplasm, cGAS perceives it as a danger signal and triggers an inflammatory response. In senescent cells, this response supports the SASP mode, in which the cell releases cytokines and other substances that change the environment around it. These experiments build on the work of Renuki Kandhaya-Pillai's group from 2017, which found that prolonged exposure to TNFα - an inflammatory signaling molecule - converted endothelial cells into senescence and maintained cytokine release through STAT proteins.
The new study asked what DNA might be the source of the cGAS signal in the same model. Researchers compared dividing cells with cells that had entered senescence due to repeated divisions or TNFα, as well as with fibroblasts from people with inherited premature aging syndromes or LMNA gene mutations. In these models, TRF2 was detected on cytoplasmic fragments near γH2AX - a protein marker of DNA damage. Prolonged TNFα treatment reduced the level of lamin B1, a nuclear envelope protein, and authors observed breaks in the envelope and the release of nuclear DNA into the cytoplasm.
🔗 Read original →
Researchers have discovered the telomere protein TRF2 on DNA fragments associated with inflammation in cells that have stopped dividing. In several models of human cells, scientists observed DNA fragments with TRF2 - a protein that protects telomeres, the ends of chromosomes - in the cytoplasm. These fragments showed signs of DNA damage and cGAS, a protein that recognizes DNA in the cytoplasm.
The nucleus normally keeps chromosomes inside the cell. When DNA enters the cytoplasm, cGAS perceives it as a danger signal and triggers an inflammatory response. In senescent cells, this response supports the SASP mode, in which the cell releases cytokines and other substances that change the environment around it. These experiments build on the work of Renuki Kandhaya-Pillai's group from 2017, which found that prolonged exposure to TNFα - an inflammatory signaling molecule - converted endothelial cells into senescence and maintained cytokine release through STAT proteins.
The new study asked what DNA might be the source of the cGAS signal in the same model. Researchers compared dividing cells with cells that had entered senescence due to repeated divisions or TNFα, as well as with fibroblasts from people with inherited premature aging syndromes or LMNA gene mutations. In these models, TRF2 was detected on cytoplasmic fragments near γH2AX - a protein marker of DNA damage. Prolonged TNFα treatment reduced the level of lamin B1, a nuclear envelope protein, and authors observed breaks in the envelope and the release of nuclear DNA into the cytoplasm.
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PubMed Central (PMC)
TRF2 enriched cytoplasmic chromatin drives cGAS-STAT1-mediated inflammation in senescence
Telomere dysfunction, persistent DNA damage, and chronic inflammation are interconnected hallmarks of cellular senescence, but their molecular links remains poorly defined. Here, we find that senescent cells accumulate telomeric protein ...
Longevity Study Results
A recent study published in Nature Medicine on August 21 analyzed 51 longevity studies with 3,128 blood samples. The authors calculated 16 epigenetic clocks, which are markers on DNA associated with age, mortality risk, or aging rate. Clinical outcomes of anti-aging interventions become apparent over years, as diseases and mortality develop slowly.
The researchers took blood samples before and after interventions and used the clocks as a rapid measure. They should notice changes and provide consistent results upon repeated measurements. The same group had previously shown that re-analyzing the same sample can be accurate, but a new sample from the same person can give a different result.
The authors collected pairs of samples before and after interventions from the TranslAGE database, unified participant information and observation periods, and recalculated the same panel of clocks for each sample. They separated the clock measurements from calendar age and compared the results for each person. This allowed them to determine which measures shifted after different interventions and in different participant groups. Measures developed to assess aging rate or mortality risk, such as DunedinPACE, more often provided a consistent response.
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A recent study published in Nature Medicine on August 21 analyzed 51 longevity studies with 3,128 blood samples. The authors calculated 16 epigenetic clocks, which are markers on DNA associated with age, mortality risk, or aging rate. Clinical outcomes of anti-aging interventions become apparent over years, as diseases and mortality develop slowly.
The researchers took blood samples before and after interventions and used the clocks as a rapid measure. They should notice changes and provide consistent results upon repeated measurements. The same group had previously shown that re-analyzing the same sample can be accurate, but a new sample from the same person can give a different result.
The authors collected pairs of samples before and after interventions from the TranslAGE database, unified participant information and observation periods, and recalculated the same panel of clocks for each sample. They separated the clock measurements from calendar age and compared the results for each person. This allowed them to determine which measures shifted after different interventions and in different participant groups. Measures developed to assess aging rate or mortality risk, such as DunedinPACE, more often provided a consistent response.
🔗 Read original →
Nature
Responsiveness of epigenetic aging biomarkers to longevity interventions in humans
Nature Medicine - The responsiveness of 16 different epigenetic aging clocks to a broad array of pharmacological and lifestyle interventions in humans was assessed across 51 different longitudinal...
IGF-1 Restores Brain Barrier
Researchers found that IGF-1 is a crucial factor in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall of old mice, both improvements weakened. This experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. The researchers evaluated the state of the barrier by introducing glowing molecules of different sizes into the blood and observing whether they exited the vessels into the brain tissue, as reported in Nature Aging, July 2026.
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Researchers found that IGF-1 is a crucial factor in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall of old mice, both improvements weakened. This experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. The researchers evaluated the state of the barrier by introducing glowing molecules of different sizes into the blood and observing whether they exited the vessels into the brain tissue, as reported in Nature Aging, July 2026.
🔗 Read original →
SpringerLink
Endothelial IGF-1/IGF-1R signaling supports young-blood-induced restoration of blood–brain barrier integrity and microvascular…
GeroScience - Aging is associated with blood–brain barrier (BBB) breakdown and microvascular rarefaction, key contributors to cerebral neuroinflammation, hypoperfusion, and vascular cognitive...
IGF-1 Key to Brain Barrier
The protein IGF-1 has been found to be a crucial link in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall in old mice, both improvements weakened. This type of experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group had already found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. In one group, IGF-1R was removed from the endothelium of the old mouse, and in another, IGF-1 production was reduced in the liver of the young partner. These interventions test different parts of the same chain. The state of the barrier was assessed through a transparent window in the skull: fluorescent molecules of different sizes were introduced into the blood, and it was observed whether they exited the vessels into the brain tissue. With a deficiency of IGF-1 or its receptor, the smallest of these molecules exited more strongly; the density of capillaries with a diameter of up to 10 micrometers also decreased. In groups with altered IGF-1 or its receptor, part of the improvements were still preserved, as reported in Nature Aging, July 2026.
🔗 Read original →
The protein IGF-1 has been found to be a crucial link in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall in old mice, both improvements weakened. This type of experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group had already found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. In one group, IGF-1R was removed from the endothelium of the old mouse, and in another, IGF-1 production was reduced in the liver of the young partner. These interventions test different parts of the same chain. The state of the barrier was assessed through a transparent window in the skull: fluorescent molecules of different sizes were introduced into the blood, and it was observed whether they exited the vessels into the brain tissue. With a deficiency of IGF-1 or its receptor, the smallest of these molecules exited more strongly; the density of capillaries with a diameter of up to 10 micrometers also decreased. In groups with altered IGF-1 or its receptor, part of the improvements were still preserved, as reported in Nature Aging, July 2026.
🔗 Read original →
SpringerLink
Endothelial IGF-1/IGF-1R signaling supports young-blood-induced restoration of blood–brain barrier integrity and microvascular…
GeroScience - Aging is associated with blood–brain barrier (BBB) breakdown and microvascular rarefaction, key contributors to cerebral neuroinflammation, hypoperfusion, and vascular cognitive...
Longer Lives in Worms
Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than typical worms, but in two groups, some of the shared genes worked in opposite directions. The authors then tested some of these genes in experiments on the animals themselves.
The study's authors first confirmed that all nine lines indeed lived longer than typical worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18. They measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell is using each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of those same genes showing decreased activity in two lines.
The authors checked whether such changes were involved in life extension, rather than just accompanying it. Out of 196 genes active in at least six lines, they were able to test 116 using RNA interference, a method that reduces the activity of a chosen gene. Most interventions did not change lifespan, but seven candidates passed a repeat test, with suppression of each reducing life in both normal worms and a line with disrupted mitochondrial function.
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Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than typical worms, but in two groups, some of the shared genes worked in opposite directions. The authors then tested some of these genes in experiments on the animals themselves.
The study's authors first confirmed that all nine lines indeed lived longer than typical worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18. They measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell is using each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of those same genes showing decreased activity in two lines.
The authors checked whether such changes were involved in life extension, rather than just accompanying it. Out of 196 genes active in at least six lines, they were able to test 116 using RNA interference, a method that reduces the activity of a chosen gene. Most interventions did not change lifespan, but seven candidates passed a repeat test, with suppression of each reducing life in both normal worms and a line with disrupted mitochondrial function.
🔗 Read original →
PubMed Central (PMC)
Multiple molecular pathways to longevity with opposing gene expression programs defining distinct aging strategies in Caenorhabditis…
While aging is the greatest risk factor for the development of neurodegenerative disease, the role of aging in these diseases is poorly understood. Our previous work has shown that targeting aging pathways can be neuroprotective in animal models of ...
Longer Life in Worms
Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than normal worms, but in two groups, some of the same genes worked in opposite directions. The authors then tested some of these genes in animal experiments.
The study found that mutations that extend life are usually studied one line at a time and under different conditions, which can reflect both biology and experimental design. The authors first confirmed that all nine lines indeed lived longer than normal worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18 samples.
The authors measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell uses each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of the same genes showing decreased activity in two lines. A similar divergence was found in genes regulated by the DAF-16/FOXO protein, which turns other genes on and off.
🔗 Read original →
Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than normal worms, but in two groups, some of the same genes worked in opposite directions. The authors then tested some of these genes in animal experiments.
The study found that mutations that extend life are usually studied one line at a time and under different conditions, which can reflect both biology and experimental design. The authors first confirmed that all nine lines indeed lived longer than normal worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18 samples.
The authors measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell uses each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of the same genes showing decreased activity in two lines. A similar divergence was found in genes regulated by the DAF-16/FOXO protein, which turns other genes on and off.
🔗 Read original →
PubMed Central (PMC)
Multiple molecular pathways to longevity with opposing gene expression programs defining distinct aging strategies in Caenorhabditis…
While aging is the greatest risk factor for the development of neurodegenerative disease, the role of aging in these diseases is poorly understood. Our previous work has shown that targeting aging pathways can be neuroprotective in animal models of ...
NSF Grants Down
The National Science Foundation (NSF) will award around 6,100 new grants, a 30% decrease from the previous year. By the end of the fiscal year, the foundation will have awarded approximately 6,100 new research grants, 46% fewer than the average from 2021-2024. This is the lowest number of new grants awarded by the NSF in over forty years.
The application process for a research grant at the NSF typically involves independent review, followed by review at a division level, which then finalizes funding. As of August 19, the foundation had awarded 5,684 new grants, with around 400 more applications pending. All new applications were due by August 3, so the estimated yearly total is around 6,100 grants.
Chemist Jarret Wilcoxen from the University of Wisconsin-Milwaukee requested equipment for his laboratory and twenty other laboratories in the region. He comments on the application process: "The applications were not rejected, but they have not been fully approved with funding either." The 43-day government shutdown at the beginning of the fiscal year delayed hundreds of panel meetings, and funding for new grants did not begin until mid-April.
In July, the foundation recalled around $300 million from two directorates, affecting over 150 applications that had already been recommended for funding. Cuts to regular NSF programs for the X-Labs initiative began earlier, and the current numbers show the scope of these cuts for the entire fiscal year. An internal NSF registry, seen by Nature, shows that $1,016,862,632 is being held from the foundation's $8.8 billion annual budget, which is not available for regular grant programs.
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The National Science Foundation (NSF) will award around 6,100 new grants, a 30% decrease from the previous year. By the end of the fiscal year, the foundation will have awarded approximately 6,100 new research grants, 46% fewer than the average from 2021-2024. This is the lowest number of new grants awarded by the NSF in over forty years.
The application process for a research grant at the NSF typically involves independent review, followed by review at a division level, which then finalizes funding. As of August 19, the foundation had awarded 5,684 new grants, with around 400 more applications pending. All new applications were due by August 3, so the estimated yearly total is around 6,100 grants.
Chemist Jarret Wilcoxen from the University of Wisconsin-Milwaukee requested equipment for his laboratory and twenty other laboratories in the region. He comments on the application process: "The applications were not rejected, but they have not been fully approved with funding either." The 43-day government shutdown at the beginning of the fiscal year delayed hundreds of panel meetings, and funding for new grants did not begin until mid-April.
In July, the foundation recalled around $300 million from two directorates, affecting over 150 applications that had already been recommended for funding. Cuts to regular NSF programs for the X-Labs initiative began earlier, and the current numbers show the scope of these cuts for the entire fiscal year. An internal NSF registry, seen by Nature, shows that $1,016,862,632 is being held from the foundation's $8.8 billion annual budget, which is not available for regular grant programs.
🔗 Read original →
Nature
Exclusive: NSF set to issue lowest number of new grants in four decades
Nature - The US science-funding agency is withholding $1 billion of its budget so that the money can go to a special White House project.
NSF Grants Reduced
The National Science Foundation (NSF) will award around 6,100 new grants, a 30% decrease from the previous year. By the end of the fiscal year, the foundation will have awarded approximately 6,100 new research grants, which is also 46% less than the average from 2021-2024. This is the lowest number of new grants awarded by the NSF in over forty years.
The application process for a research grant at the NSF typically involves independent review, followed by review at a division level, where funding is finalized. As of August 19, the foundation had awarded 5,684 new grants, with around 400 more applications pending. All new applications were due by August 3, so the estimated yearly total is around 6,100 grants.
A 43-day government shutdown at the beginning of the fiscal year delayed hundreds of panel meetings, and funding for new grants did not begin until mid-April. In July, the foundation withdrew around $300 million from two directorates, affecting more than 150 applications that had already been recommended for funding. Cuts to regular NSF programs in favor of the X-Labs initiative began earlier, and the current numbers show the scale of these cuts for the entire fiscal year.
According to an internal NSF registry obtained by Nature, $1,016,862,632 is being held on the central account from the foundation's $8.8 billion yearly budget. These funds are not available for regular grant programs. A significant portion of the pool is being directed towards the White House's Grand Research Challenges initiative, which includes large research challenges in areas such as artificial intelligence and advanced materials.
🔗 Read original →
The National Science Foundation (NSF) will award around 6,100 new grants, a 30% decrease from the previous year. By the end of the fiscal year, the foundation will have awarded approximately 6,100 new research grants, which is also 46% less than the average from 2021-2024. This is the lowest number of new grants awarded by the NSF in over forty years.
The application process for a research grant at the NSF typically involves independent review, followed by review at a division level, where funding is finalized. As of August 19, the foundation had awarded 5,684 new grants, with around 400 more applications pending. All new applications were due by August 3, so the estimated yearly total is around 6,100 grants.
A 43-day government shutdown at the beginning of the fiscal year delayed hundreds of panel meetings, and funding for new grants did not begin until mid-April. In July, the foundation withdrew around $300 million from two directorates, affecting more than 150 applications that had already been recommended for funding. Cuts to regular NSF programs in favor of the X-Labs initiative began earlier, and the current numbers show the scale of these cuts for the entire fiscal year.
According to an internal NSF registry obtained by Nature, $1,016,862,632 is being held on the central account from the foundation's $8.8 billion yearly budget. These funds are not available for regular grant programs. A significant portion of the pool is being directed towards the White House's Grand Research Challenges initiative, which includes large research challenges in areas such as artificial intelligence and advanced materials.
🔗 Read original →
Nature
Exclusive: NSF set to issue lowest number of new grants in four decades
Nature - The US science-funding agency is withholding $1 billion of its budget so that the money can go to a special White House project.
Pixelgen Funding
Pixelgen has raised $15.5 million to commercialize the measurement of protein neighborhood on the surface of individual cells. On August 20, Pixelgen announced a Series B round of $15.5 million, led by Flat Capital, with existing investors Industrifonden and Navigare Ventures participating. The company will use the funds for global commercialization of the Proxiome Kit, team expansion, and product portfolio growth.
The surface of a cell contains proteins that receive external signals and respond to them. Traditional single-cell analysis counts which proteins are present in a cell and how many there are. The Proxiome Kit adds arrangement information: which proteins cluster together and which are nearby on the cell membrane. The kit is based on the Proximity Network Assay. Cells are fixed, then antibodies with DNA barcodes bind to selected surface proteins. The barcodes are copied multiple times near the binding site, and neighboring copies are connected and read by sequencing - a method of reading DNA sequences.
In a preprint, the authors described a panel of 155 plasma membrane proteins and applied the method to blood cells, blood cancer cell lines, CAR-T models, and autoimmune disease samples. In one cell, they obtained tens of thousands of spatial nodes and around 12 thousand pairwise relationships between proteins. A single sample provides both a traditional list of protein markers and a scheme of their neighborhood on the cell surface. Pixelgen is bringing this measurement method to a commercial kit, as described in preprint, August 2026. Laboratories will be able to compare cells not only by their protein set but also by how these proteins are arranged next to each other.
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Pixelgen has raised $15.5 million to commercialize the measurement of protein neighborhood on the surface of individual cells. On August 20, Pixelgen announced a Series B round of $15.5 million, led by Flat Capital, with existing investors Industrifonden and Navigare Ventures participating. The company will use the funds for global commercialization of the Proxiome Kit, team expansion, and product portfolio growth.
The surface of a cell contains proteins that receive external signals and respond to them. Traditional single-cell analysis counts which proteins are present in a cell and how many there are. The Proxiome Kit adds arrangement information: which proteins cluster together and which are nearby on the cell membrane. The kit is based on the Proximity Network Assay. Cells are fixed, then antibodies with DNA barcodes bind to selected surface proteins. The barcodes are copied multiple times near the binding site, and neighboring copies are connected and read by sequencing - a method of reading DNA sequences.
In a preprint, the authors described a panel of 155 plasma membrane proteins and applied the method to blood cells, blood cancer cell lines, CAR-T models, and autoimmune disease samples. In one cell, they obtained tens of thousands of spatial nodes and around 12 thousand pairwise relationships between proteins. A single sample provides both a traditional list of protein markers and a scheme of their neighborhood on the cell surface. Pixelgen is bringing this measurement method to a commercial kit, as described in preprint, August 2026. Laboratories will be able to compare cells not only by their protein set but also by how these proteins are arranged next to each other.
🔗 Read original →
Viral Gene Therapy
Researchers have used a viral vector to deliver a working copy of the ALPK3 gene to heart cells in adult mice with a inherited heart muscle disease. The study, published in Nature Cardiovascular Research on August 19, found that the treatment restored heart function and structure to levels similar to those of healthy animals.
The heart contracts due to sarcomeres, repeating protein structures in muscle cells, and ALPK3 helps maintain these proteins in working condition. Without two working copies of ALPK3, the heart becomes enlarged and pumps blood less efficiently. In humans, disease-causing variants of this gene lead to inherited cardiomyopathies, with ALPK3 variants accounting for around 2% of cases of hypertrophic cardiomyopathy.
The researchers used an AAV viral vector to package a 5,800-base pair construct containing ALPK3, and found that it restored order to the contraction apparatus in diseased hearts. They also tested the therapy in human heart organoids with variants of the TTN gene, which codes for the massive protein titin that forms the sarcomere framework. The results showed that delivering ALPK3 restored contraction strength to levels similar to those of organoids without the variant.
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Researchers have used a viral vector to deliver a working copy of the ALPK3 gene to heart cells in adult mice with a inherited heart muscle disease. The study, published in Nature Cardiovascular Research on August 19, found that the treatment restored heart function and structure to levels similar to those of healthy animals.
The heart contracts due to sarcomeres, repeating protein structures in muscle cells, and ALPK3 helps maintain these proteins in working condition. Without two working copies of ALPK3, the heart becomes enlarged and pumps blood less efficiently. In humans, disease-causing variants of this gene lead to inherited cardiomyopathies, with ALPK3 variants accounting for around 2% of cases of hypertrophic cardiomyopathy.
The researchers used an AAV viral vector to package a 5,800-base pair construct containing ALPK3, and found that it restored order to the contraction apparatus in diseased hearts. They also tested the therapy in human heart organoids with variants of the TTN gene, which codes for the massive protein titin that forms the sarcomere framework. The results showed that delivering ALPK3 restored contraction strength to levels similar to those of organoids without the variant.
🔗 Read original →
Nature
Alpha protein kinase 3 gene therapy restores heart function in mouse and human models of cardiomyopathy
Nature Cardiovascular Research - McNamara et al. demonstrate that adeno-associated virus-mediated delivery of full-length human ALPK3 prevents cardiomyopathy in neonatal mouse models and reverses...
Cas9d Ultra Editor
The compact Cas9d Ultra editor was placed in a single AAV viral vector and used to modify a gene in the livers of mice. On August 19, authors published a study on Cas9d Ultra, a compact genetic editor. One of its variants, 9dCBE, changes the letter C in DNA; it was packaged with a guide RNA in a single AAV9 viral vector and administered to newborn mice.
Through five weeks, the editor modified the target region of the Pcsk9 gene in the liver by an average of 15.7%, and the level of LDL cholesterol in the serum was lower than in mice after PBS injection. The base editor makes precise changes to one "letter" of DNA. The guide RNA sets the address in the genome, the CRISPR protein holds the editor in place, and the attached enzyme performs the chemical replacement of the base.
The AAV virus, which carries the genetic cargo into cells, typically holds around 4,700 nucleotides. Large editors are often split between two vectors. In this study, a single AAV9 delivered both the editor and its guide RNA. The Cas9d MG34-1 was chosen due to its size: this protein consists of 747 amino acids and works with a guide RNA of normal length for CRISPR. In a 2022 study, its early version achieved up to 22% base editing on three targets in human cells. The current authors modified four amino acids in the protein and the guide RNA scaffold. In a cellular test, where DNA cutting triggers a fluorescent signal, activity increased from 20.44% to 63.32%.
🔗 Read original →
The compact Cas9d Ultra editor was placed in a single AAV viral vector and used to modify a gene in the livers of mice. On August 19, authors published a study on Cas9d Ultra, a compact genetic editor. One of its variants, 9dCBE, changes the letter C in DNA; it was packaged with a guide RNA in a single AAV9 viral vector and administered to newborn mice.
Through five weeks, the editor modified the target region of the Pcsk9 gene in the liver by an average of 15.7%, and the level of LDL cholesterol in the serum was lower than in mice after PBS injection. The base editor makes precise changes to one "letter" of DNA. The guide RNA sets the address in the genome, the CRISPR protein holds the editor in place, and the attached enzyme performs the chemical replacement of the base.
The AAV virus, which carries the genetic cargo into cells, typically holds around 4,700 nucleotides. Large editors are often split between two vectors. In this study, a single AAV9 delivered both the editor and its guide RNA. The Cas9d MG34-1 was chosen due to its size: this protein consists of 747 amino acids and works with a guide RNA of normal length for CRISPR. In a 2022 study, its early version achieved up to 22% base editing on three targets in human cells. The current authors modified four amino acids in the protein and the guide RNA scaffold. In a cellular test, where DNA cutting triggers a fluorescent signal, activity increased from 20.44% to 63.32%.
🔗 Read original →
PubMed Central (PMC)
Compact 9dBEs Enable Efficient and Precise Genome Editing in Mammalian Cells and In Vivo
Despite the promise of DNA base editors for diverse genome editing applications, their utility remains constrained by off‐target effects, which are exacerbated by short spacers in miniature systems and the large size of Cas9‐derived editors, which ...
Jacek Hoffmann Proposal
Jacek Hoffmann proposed building systems from multiple AI agents with different data and verification methods. On August 20, Hoffmann published an essay on "heterogeneous cognitive ecology": humans and AI approach a task with different methods and data, then cross-check results. He calls the scenario where multiple agents share one mistake "Beryl Cage".
Hoffmann assumes a possible asymmetry: AI systems will increasingly create and transform information, while an individual will find it harder to reconstruct the solution path. He sees a sample verification device in science: one participant proposes an explanation, another looks for a counterexample, and a third repeats the analysis with different data or methods. This makes the error more noticeable where the results diverge.
Diverging data, methods, and criteria create different reasoning paths and different errors. The divergence can reveal a hidden assumption or condition that the first participant missed. Ten copies of one system can agree because they err in the same way. "The number of models is not equal to diversity," Hoffmann writes, citing an official report from Anthropic, August 13.
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Jacek Hoffmann proposed building systems from multiple AI agents with different data and verification methods. On August 20, Hoffmann published an essay on "heterogeneous cognitive ecology": humans and AI approach a task with different methods and data, then cross-check results. He calls the scenario where multiple agents share one mistake "Beryl Cage".
Hoffmann assumes a possible asymmetry: AI systems will increasingly create and transform information, while an individual will find it harder to reconstruct the solution path. He sees a sample verification device in science: one participant proposes an explanation, another looks for a counterexample, and a third repeats the analysis with different data or methods. This makes the error more noticeable where the results diverge.
Diverging data, methods, and criteria create different reasoning paths and different errors. The divergence can reveal a hidden assumption or condition that the first participant missed. Ten copies of one system can agree because they err in the same way. "The number of models is not equal to diversity," Hoffmann writes, citing an official report from Anthropic, August 13.
🔗 Read original →
Substack
Prisoners of the Stone Age in a World of Exabytes
From the Biological Limits of Mind to a Heterogeneous Cognitive Ecology
AC Immune Reports Progress
AC Immune reported that ACI-19764 reached the cerebrospinal fluid around the brain and dose-dependently suppressed the inflammatory signal IL-1β in blood analysis. On August 20, AC Immune published interim data from the first cohorts of the ACI-19764 study in healthy volunteers. The company checked if the drug reached the central nervous system environment, achieved the necessary concentration there, and was associated with a biochemical response in the blood.
The ACI-19764 is an orally administered small chemical compound. AC Immune is developing it as an NLRP3-inflammasome inhibitor - an intracellular complex of the immune system involved in the formation of inflammatory signals, including IL-1β. In the August 20 release, the company reported on cohorts with single and repeated doses. The detection of ACI-19764 in cerebrospinal fluid shows that the drug reached the central nervous system environment.
Daily doses of up to 10 mg gave concentrations above the IC90 level - the level of substance that in a laboratory test suppresses 90% of the chosen response. In whole blood samples, IL-1β release decreased with increasing dose. These measurements answer different questions: did the drug reach the central nervous system environment, is its concentration sufficient for the laboratory goal, and does IL-1β release in the blood decrease with dose. The original protocol in the NCT07463196 registry is designed for 78 healthy volunteers.
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AC Immune reported that ACI-19764 reached the cerebrospinal fluid around the brain and dose-dependently suppressed the inflammatory signal IL-1β in blood analysis. On August 20, AC Immune published interim data from the first cohorts of the ACI-19764 study in healthy volunteers. The company checked if the drug reached the central nervous system environment, achieved the necessary concentration there, and was associated with a biochemical response in the blood.
The ACI-19764 is an orally administered small chemical compound. AC Immune is developing it as an NLRP3-inflammasome inhibitor - an intracellular complex of the immune system involved in the formation of inflammatory signals, including IL-1β. In the August 20 release, the company reported on cohorts with single and repeated doses. The detection of ACI-19764 in cerebrospinal fluid shows that the drug reached the central nervous system environment.
Daily doses of up to 10 mg gave concentrations above the IC90 level - the level of substance that in a laboratory test suppresses 90% of the chosen response. In whole blood samples, IL-1β release decreased with increasing dose. These measurements answer different questions: did the drug reach the central nervous system environment, is its concentration sufficient for the laboratory goal, and does IL-1β release in the blood decrease with dose. The original protocol in the NCT07463196 registry is designed for 78 healthy volunteers.
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PubMed Central (PMC)
First‐in‐human safety, tolerability, and pharmacokinetic results of DFV890, an oral low‐molecular‐weight NLRP3 inhibitor
This first‐in‐human study evaluated the safety, tolerability, single‐ and multiple‐dose pharmacokinetic profiles with dietary influence, and pharmacodynamics (PD) of DFV890, an oral NLRP3 inhibitor, in healthy participants. In total, 122 ...
Perturb-ME Maps Cell Mechanisms
Researchers from Genentech and the Broad Institute presented the Perturb-ME method in a preprint on August 18, which combines genome-wide CRISPR knockout with cell sorting and single-cell analysis to build maps of cell mechanisms. The approach combines genome-wide gene knockout with cell sorting by target protein level and simultaneous reading of the knocked-out gene, RNA, and surface markers in each cell.
In an experiment on melanoma cells, the authors reconstructed a regulatory network of 221 regulator genes and 1998 response genes, and deposited the code and computational pipelines in an open repository. The main obstacle in studying complex cellular processes remains the gap between arrays of genetic correlations and testable causal links. When biologists want to determine how each individual gene controls a trait, they have to choose between two extremes.
The new Perturb-ME approach (Perturb-seq with Marker Enrichment) overcomes this limitation with a two-step design. First, genes are knocked out across the genome in a pool of cells using the CRISPR system. Then, the population is passed through a flow cytometer, selecting only the top and bottom 5% of cells with the minimum and maximum levels of the protein of interest. This step filters out cells without an expressed response and concentrates the effective mutations.
Only after this cell sorting step are the cells sent for multimodal single-cell profiling. Within each cell, the guiding RNA, transcriptome, and level of surface proteins are read simultaneously using DNA-barcoded antibodies. The work of the method was verified using the example of the major histocompatibility complex I (MHC-I) in human melanoma cells, and the results were published in Nature Aging, July 2026.
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Researchers from Genentech and the Broad Institute presented the Perturb-ME method in a preprint on August 18, which combines genome-wide CRISPR knockout with cell sorting and single-cell analysis to build maps of cell mechanisms. The approach combines genome-wide gene knockout with cell sorting by target protein level and simultaneous reading of the knocked-out gene, RNA, and surface markers in each cell.
In an experiment on melanoma cells, the authors reconstructed a regulatory network of 221 regulator genes and 1998 response genes, and deposited the code and computational pipelines in an open repository. The main obstacle in studying complex cellular processes remains the gap between arrays of genetic correlations and testable causal links. When biologists want to determine how each individual gene controls a trait, they have to choose between two extremes.
The new Perturb-ME approach (Perturb-seq with Marker Enrichment) overcomes this limitation with a two-step design. First, genes are knocked out across the genome in a pool of cells using the CRISPR system. Then, the population is passed through a flow cytometer, selecting only the top and bottom 5% of cells with the minimum and maximum levels of the protein of interest. This step filters out cells without an expressed response and concentrates the effective mutations.
Only after this cell sorting step are the cells sent for multimodal single-cell profiling. Within each cell, the guiding RNA, transcriptome, and level of surface proteins are read simultaneously using DNA-barcoded antibodies. The work of the method was verified using the example of the major histocompatibility complex I (MHC-I) in human melanoma cells, and the results were published in Nature Aging, July 2026.
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bioRxiv
Perturb-ME: Scalable mechanism discovery from phenotype-enriched genome-wide screens
Perturb-seq enables pooled genetic screens with rich single-cell profiling readouts, but genome-scale profiling remains costly and may not be associated with other established functional characteristics. Moreover, as screens grow in size and complexity, interpreting…
UK Clinical Trials
The UK has published clinical trial metrics, with 82% of already open studies recruiting participants on schedule, but launch after approval is lagging. On August 19, the UK's Department of Health and Social Care published July metrics for the UKCRD program, which tracks clinical trial timelines.
The program measures the path from application to first participant separately, including the stages of regulatory and ethics committee approval, research center opening, and first participant enrollment. The 82% metric describes recruitment in already open studies, while launch after approval is measured by separate metrics.
In the CPMS registry, a database of the UK's National Institute for Health and Care Research network, there were 4,347 open studies in July, with 82% of them recruiting on schedule and reaching target participant numbers, exceeding the 80% goal. The UKCRD has been publishing these metrics since 2024.
For commercial drug trials, a 150-day metric covers the entire path from application to first participant, with all nine January-submitted studies meeting this timeline. After approval, the report tracks two more stages: 56% of studies opened recruitment within 60 days, and 61% enrolled their first participant within 30 days of opening recruitment, with a 90% goal for both stages, as reported in the UKCRD July metrics.
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The UK has published clinical trial metrics, with 82% of already open studies recruiting participants on schedule, but launch after approval is lagging. On August 19, the UK's Department of Health and Social Care published July metrics for the UKCRD program, which tracks clinical trial timelines.
The program measures the path from application to first participant separately, including the stages of regulatory and ethics committee approval, research center opening, and first participant enrollment. The 82% metric describes recruitment in already open studies, while launch after approval is measured by separate metrics.
In the CPMS registry, a database of the UK's National Institute for Health and Care Research network, there were 4,347 open studies in July, with 82% of them recruiting on schedule and reaching target participant numbers, exceeding the 80% goal. The UKCRD has been publishing these metrics since 2024.
For commercial drug trials, a 150-day metric covers the entire path from application to first participant, with all nine January-submitted studies meeting this timeline. After approval, the report tracks two more stages: 56% of studies opened recruitment within 60 days, and 61% enrolled their first participant within 30 days of opening recruitment, with a 90% goal for both stages, as reported in the UKCRD July metrics.
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GOV.UK
UK Clinical Research Delivery key performance indicators: data to July 2026
The UK Clinical Research Delivery (UKCRD) key performance indicators (KPIs) report brings together data from the National Institute for Health and Care Research (NIHR) and the Medicines and Healthcare products Regulatory Agency (MHRA) to monitor the delivery…
Blood Age Shift
A recent analysis of 48 DNA segments found that changes in immune cells explained most of the decade-long shift in blood methylation. On August 19, a preprint was published with paired blood samples from 86 elderly participants over ten years. After accounting for the estimated change in immune cell composition, 32.2% of the original rate of shift in the 48-segment metric remained; this residue was not statistically different from zero.
Methylation refers to chemical marks on DNA, which are used to build epigenetic age indicators. However, a blood test always contains a mixture of immune cells, each with their own methylation patterns. If the proportions of these cells change over the years, the average blood signal shifts, even without a similar shift within each cell type. The preprint author took a metric from 48 preselected DNA segments and tracked it in two longitudinal cohorts.
For the Danish cohort of 86 participants, the author estimated changes in the proportions of seven types of immune cells using a separate set of DNA markers and included these changes in the calculation. The rate of shift in the metric dropped to 32.2% of the original, and the model with changing cell composition explained 36.4% of the variance in metric change between participants. Comparing a person to themselves removes their constant features, including their usual blood composition, which can change over ten years.
In a 2024 study, the IntrinClock model was calibrated so that its readings did not change between ten validated types of immune cells. In purified naive CD8+ T cells, its metric still increased with age. Reanalysis of blood should show the shift in immune composition and what remains after such correction separately. Then, one figure does not mix the rearrangement of cells with the change in marks within them, as reported in Nature Aging, July 2026.
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A recent analysis of 48 DNA segments found that changes in immune cells explained most of the decade-long shift in blood methylation. On August 19, a preprint was published with paired blood samples from 86 elderly participants over ten years. After accounting for the estimated change in immune cell composition, 32.2% of the original rate of shift in the 48-segment metric remained; this residue was not statistically different from zero.
Methylation refers to chemical marks on DNA, which are used to build epigenetic age indicators. However, a blood test always contains a mixture of immune cells, each with their own methylation patterns. If the proportions of these cells change over the years, the average blood signal shifts, even without a similar shift within each cell type. The preprint author took a metric from 48 preselected DNA segments and tracked it in two longitudinal cohorts.
For the Danish cohort of 86 participants, the author estimated changes in the proportions of seven types of immune cells using a separate set of DNA markers and included these changes in the calculation. The rate of shift in the metric dropped to 32.2% of the original, and the model with changing cell composition explained 36.4% of the variance in metric change between participants. Comparing a person to themselves removes their constant features, including their usual blood composition, which can change over ten years.
In a 2024 study, the IntrinClock model was calibrated so that its readings did not change between ten validated types of immune cells. In purified naive CD8+ T cells, its metric still increased with age. Reanalysis of blood should show the shift in immune composition and what remains after such correction separately. Then, one figure does not mix the rearrangement of cells with the change in marks within them, as reported in Nature Aging, July 2026.
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Brain Ultrasound
The SonoMod module attaches to a mouse's head, focusing ultrasound on a brain area while simultaneously recording its response with a miniature camera. On August 18, authors published a preprint on SonoMod, releasing files for assembly, optics, analysis software, and data. Focused ultrasound concentrates sound wave energy in a small brain point.
The device allows for simultaneous stimulation and recording, overcoming previous setup limitations that required head fixation or separate sessions for stimulation and recording. According to the authors, "in neuroscience, tools for intervening in neural circuits and reading their response have traditionally relied on incompatible physics." In SonoMod, light and sound pass through a single module, with a transparent niobate disk converting an electrical signal into ultrasound.
The UCLA Miniscope v4, an open miniature microscope for experiments with freely moving animals, is used with the SonoMod module. Authors tested the device in a series of experiments, first verifying that the camera can see the brain through the module, and then directing ultrasound to the secondary motor cortex (M2). The results were published in a preprint repository and are awaiting review in a neuroscience journal.
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The SonoMod module attaches to a mouse's head, focusing ultrasound on a brain area while simultaneously recording its response with a miniature camera. On August 18, authors published a preprint on SonoMod, releasing files for assembly, optics, analysis software, and data. Focused ultrasound concentrates sound wave energy in a small brain point.
The device allows for simultaneous stimulation and recording, overcoming previous setup limitations that required head fixation or separate sessions for stimulation and recording. According to the authors, "in neuroscience, tools for intervening in neural circuits and reading their response have traditionally relied on incompatible physics." In SonoMod, light and sound pass through a single module, with a transparent niobate disk converting an electrical signal into ultrasound.
The UCLA Miniscope v4, an open miniature microscope for experiments with freely moving animals, is used with the SonoMod module. Authors tested the device in a series of experiments, first verifying that the camera can see the brain through the module, and then directing ultrasound to the secondary motor cortex (M2). The results were published in a preprint repository and are awaiting review in a neuroscience journal.
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PubMed Central (PMC)
General‐Purpose Ultrasound Neuromodulation System for Chronic, Closed‐Loop Preclinical Studies in Freely Behaving Rodents
Transcranial focused ultrasound stimulation (tFUS) is an effective noninvasive treatment modality for brain disorders with high clinical potential. However, the therapeutic effects of ultrasound neuromodulation are not widely explored due to ...
Virtual Gene Knockout
The authors of a preprint compared eight methods that attempt to predict the consequences of gene knockout based on single-cell RNA data. In a test on K562 leukemia cells, the direction predicted by the linear version of CellOracle matched the experiment in 18 out of 44 "transcription factor — gene" pairs. The data on single-cell RNA shows which genes are usually active together, allowing researchers to build a hypothesis about the regulatory network and choose a gene for the next experiment.
The actual gene knockout answers a different question: how will the work of each specific gene change after intervention. The authors tested four transcription factors — proteins that control the work of other genes — and 11 glycolysis genes, the first stage of a cell obtaining energy from glucose. In Perturb-seq, researchers use CRISPRi to suppress the work of a selected gene and then read the RNA of individual cells. The average activity of these 11 genes decreased in all four factors.
The measurements were then compared to the signs of coefficients in the linear version of CellOracle. The sign of the coefficient describes the relationship between genes in the RNA data, and CRISPRi shows their response to intervention. The directions matched in 18 out of 44 cases, as reported in the preprint of August 19.
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The authors of a preprint compared eight methods that attempt to predict the consequences of gene knockout based on single-cell RNA data. In a test on K562 leukemia cells, the direction predicted by the linear version of CellOracle matched the experiment in 18 out of 44 "transcription factor — gene" pairs. The data on single-cell RNA shows which genes are usually active together, allowing researchers to build a hypothesis about the regulatory network and choose a gene for the next experiment.
The actual gene knockout answers a different question: how will the work of each specific gene change after intervention. The authors tested four transcription factors — proteins that control the work of other genes — and 11 glycolysis genes, the first stage of a cell obtaining energy from glucose. In Perturb-seq, researchers use CRISPRi to suppress the work of a selected gene and then read the RNA of individual cells. The average activity of these 11 genes decreased in all four factors.
The measurements were then compared to the signs of coefficients in the linear version of CellOracle. The sign of the coefficient describes the relationship between genes in the RNA data, and CRISPRi shows their response to intervention. The directions matched in 18 out of 44 cases, as reported in the preprint of August 19.
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AI Model Helps Find Gene
Researchers combined an AI model with data on gene activity in individual blood stem cells, genetic regulator testing, and cell transplantation in mice. They found that the Pbx1 gene is involved in the age-related shift: after transplantation, old cells are less effective at restoring erythrocytes and more likely to produce thrombocyte precursors.
The study, published on August 21 in Science Advances, used the Geneformer AI model to identify the Pbx1 gene as a key regulator of this shift. The model was trained on ten datasets of young and old mouse HSC cells and used to predict which genes, when activated, would make young cells resemble old cells.
The team then tested the prediction in cells by activating 143 genetic regulators associated with blood formation in young HSC cells and tracking the CD48 marker. They found that increased Pbx1 activity slowed the appearance of CD48, and that its activity was higher in old HSC cells.
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Researchers combined an AI model with data on gene activity in individual blood stem cells, genetic regulator testing, and cell transplantation in mice. They found that the Pbx1 gene is involved in the age-related shift: after transplantation, old cells are less effective at restoring erythrocytes and more likely to produce thrombocyte precursors.
The study, published on August 21 in Science Advances, used the Geneformer AI model to identify the Pbx1 gene as a key regulator of this shift. The model was trained on ten datasets of young and old mouse HSC cells and used to predict which genes, when activated, would make young cells resemble old cells.
The team then tested the prediction in cells by activating 143 genetic regulators associated with blood formation in young HSC cells and tracking the CD48 marker. They found that increased Pbx1 activity slowed the appearance of CD48, and that its activity was higher in old HSC cells.
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PubMed Central (PMC)
Geneformer-guided multiomics integration identifies Pbx1 as a network hub of hematopoietic stem cell aging
Hematopoietic stem cells (HSCs) constitute an organized hematopoietic system that undergoes age-related alterations, including increased platelet production and decreased erythropoiesis. The fundamental mechanisms driving these shifts remain ...
Mambbot Project
Molecular biologist Майкл Левин proposes using a series of AI-driven experiments to search for the desired form of living tissue. On 21 августа, he released a lecture on "free lunches," where he describes Mambbot, a collaborative project that uses AI to suggest light, vibration, temperature, or chemical signals to apply to cells to search for a biobot with a specific form and function.
The concept of a "free lunch" refers to the gap between what a system provides and the effort explicitly invested in it through design, selection, or training. According to Levin, this gap defines the next experiment: what property of the system produced the result, and how can it be induced again. This idea grows out of his laboratory's long-standing work at Университете Тафтса on morphogenesis, or how cellular collectives assemble, repair, and change body shape.
In a 2021 article, the authors described ksenobots, mobile constructs made from frog embryo cells. These clusters assembled free cells into new clusters, and an algorithm selected forms that reproduced better. In work on anthrobots, adult human airway cells self-organized into mobile constructs, and in neural cultures, they accelerated the closure of damaged areas. These results provided researchers with a material in which to observe the form and function of cellular collectives after changing conditions.
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Molecular biologist Майкл Левин proposes using a series of AI-driven experiments to search for the desired form of living tissue. On 21 августа, he released a lecture on "free lunches," where he describes Mambbot, a collaborative project that uses AI to suggest light, vibration, temperature, or chemical signals to apply to cells to search for a biobot with a specific form and function.
The concept of a "free lunch" refers to the gap between what a system provides and the effort explicitly invested in it through design, selection, or training. According to Levin, this gap defines the next experiment: what property of the system produced the result, and how can it be induced again. This idea grows out of his laboratory's long-standing work at Университете Тафтса on morphogenesis, or how cellular collectives assemble, repair, and change body shape.
In a 2021 article, the authors described ksenobots, mobile constructs made from frog embryo cells. These clusters assembled free cells into new clusters, and an algorithm selected forms that reproduced better. In work on anthrobots, adult human airway cells self-organized into mobile constructs, and in neural cultures, they accelerated the closure of damaged areas. These results provided researchers with a material in which to observe the form and function of cellular collectives after changing conditions.
🔗 Read original →
PubMed Central (PMC)
Kinematic self-replication in reconfigurable organisms
Almost all organisms replicate by growing and then shedding offspring. Some molecules also replicate, but by moving rather than growing: They find and combine building blocks into self-copies. Here we show that clusters of cells, if freed from a ...