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.
🔗 Read original →
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.
🔗 Read original →
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.
🔗 Read original →
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.
🔗 Read original →
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...
New Theory of Aging
Researchers Michael Levin and co-authors proposed a third theory of aging, where cells lose their common goal to maintain tissue shape. On August 18, Leo Pió-López, Navnit Javanda, and Michael Levin published a preprint review of aging theories. The authors group these theories by their presumed primary cause: accumulation of damage, late consequences of evolutionary programs, and loss of coordinated cell purpose in tissue.
The authors' own theoretical model describes how cells maintain the overall structure of tissue. By "purpose," the authors mean the work of feedback: cells compare the current state of tissue with its target structure and reduce the discrepancy. During development, this process creates the body's form. According to the authors' model, after development is complete, cells may maintain their local functions but poorly coordinate repair, growth, and cell replacement with the organ's form.
One possible carrier of such coordination, the authors consider, is bioelectric patterns - the distribution of electrical potentials in tissue. The review also mentions chemical signals and mechanical properties of tissue. If cells poorly maintain or read the common scheme of signals, the tissue, according to the authors' hypothesis, deviates from the necessary structure and function, as seen in Nature Aging, July 2026.
🔗 Read original →
Researchers Michael Levin and co-authors proposed a third theory of aging, where cells lose their common goal to maintain tissue shape. On August 18, Leo Pió-López, Navnit Javanda, and Michael Levin published a preprint review of aging theories. The authors group these theories by their presumed primary cause: accumulation of damage, late consequences of evolutionary programs, and loss of coordinated cell purpose in tissue.
The authors' own theoretical model describes how cells maintain the overall structure of tissue. By "purpose," the authors mean the work of feedback: cells compare the current state of tissue with its target structure and reduce the discrepancy. During development, this process creates the body's form. According to the authors' model, after development is complete, cells may maintain their local functions but poorly coordinate repair, growth, and cell replacement with the organ's form.
One possible carrier of such coordination, the authors consider, is bioelectric patterns - the distribution of electrical potentials in tissue. The review also mentions chemical signals and mechanical properties of tissue. If cells poorly maintain or read the common scheme of signals, the tissue, according to the authors' hypothesis, deviates from the necessary structure and function, as seen in Nature Aging, July 2026.
🔗 Read original →
PubMed Central (PMC)
Aging as a Loss of Goal‐Directedness: An Evolutionary Simulation and Analysis Unifying Regeneration with Anatomical Rejuvenation
Although substantial advancements are made in manipulating lifespan in model organisms, the fundamental mechanisms driving aging remain elusive. No comprehensive computational platform is capable of making predictions on aging in multicellular ...
Merck and Moderna Report Success
Merck and Moderna reported on August 19 the results of the INTerpath-001 phase III study with 1,137 participants. After complete removal of high-risk melanoma, all participants received pembrolizumab: one group was also given a personally tailored intismeran, while the other received a placebo.
The companies reported that the combination achieved two study goals: time without recurrence and time without distant metastases. After melanoma removal, the risk of its return remains. Pembrolizumab is an immunotherapy that blocks the PD-1 protein, which reduces the activity of T-cells that can attack tumors. Intismeran gives these cells specific targets.
According to oncologist Lennard Lee, as quoted in the Science Media Centre, the combination of the two drugs works by "one helping the immune system understand what to look for, and the other taking the brakes off the immune response". For intismeran, a tumor sample from a specific patient is taken, and up to 34 neoantigens - fragments of proteins that distinguish cancer cells from healthy ones - are selected. Their sequences are recorded in mRNA: after injection, the patient's cells produce these fragments and show them to T-cells.
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Merck and Moderna reported on August 19 the results of the INTerpath-001 phase III study with 1,137 participants. After complete removal of high-risk melanoma, all participants received pembrolizumab: one group was also given a personally tailored intismeran, while the other received a placebo.
The companies reported that the combination achieved two study goals: time without recurrence and time without distant metastases. After melanoma removal, the risk of its return remains. Pembrolizumab is an immunotherapy that blocks the PD-1 protein, which reduces the activity of T-cells that can attack tumors. Intismeran gives these cells specific targets.
According to oncologist Lennard Lee, as quoted in the Science Media Centre, the combination of the two drugs works by "one helping the immune system understand what to look for, and the other taking the brakes off the immune response". For intismeran, a tumor sample from a specific patient is taken, and up to 34 neoantigens - fragments of proteins that distinguish cancer cells from healthy ones - are selected. Their sequences are recorded in mRNA: after injection, the patient's cells produce these fragments and show them to T-cells.
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Merck.com
Merck and Moderna Announce Phase 3 INTerpath-001 Trial of Intismeran Autogene Plus KEYTRUDA® Met Endpoints of Recurrence-Free Survival…
First and only combination regimen to demonstrate statistically significant and clinically meaningful improvements in RFS and DMFS compared to KEYTRUDA alone for these patients in the adjuvant melanoma setting The Companies plan to present data at an upcoming…
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Longevity Interventions
Яцек Хоффман proposes selecting combinations of anti-aging interventions based on the current state of the organism. On August 19, Яцек Хоффман published an essay with his author's hypothesis: to maintain health throughout a long life, it is necessary to evaluate several processes at once and select their combination based on the state of the organism. The starting point for Хоффман was a study on the heart of the Greenland shark. The authors studied the tissues of ten sharks aged approximately 100-155 years and found fibrosis, lipofuscin, and signs of oxidative stress.
Before capture, the animals were found, chased, and caught with bait; the authors consider this indirect evidence of preserved physiological function. Хоффман takes the discrepancy between tissue damage and active behavior of the sharks as a reason to question this in humans. In his hypothesis, the organism must maintain several processes at once, and enhancing one changes the conditions for the others.
Active removal of damaged cells helps to restrain tumors, but increases the tissue's need for restoration. Stem cells replenish lost cells; the more they divide, the more the tissue is renewed and the more opportunities there are for changes in individual cells. The immune system recognizes infections and anomalous cells, and its prolonged activation damages tissues. One intervention changes the work of other systems.
Therefore, Хоффман proposes choosing an intervention based on age, specific tissue, accumulated damage, and resource reserve. His sequence of actions looks like this: "Observation → reconstruction of the current state → causal model → selection of intervention → action → repeated measurement → model update". Хоффман proposes testing this hypothesis by comparing models, such as those described in Nature Aging, July 2026.
🔗 Read original →
Яцек Хоффман proposes selecting combinations of anti-aging interventions based on the current state of the organism. On August 19, Яцек Хоффман published an essay with his author's hypothesis: to maintain health throughout a long life, it is necessary to evaluate several processes at once and select their combination based on the state of the organism. The starting point for Хоффман was a study on the heart of the Greenland shark. The authors studied the tissues of ten sharks aged approximately 100-155 years and found fibrosis, lipofuscin, and signs of oxidative stress.
Before capture, the animals were found, chased, and caught with bait; the authors consider this indirect evidence of preserved physiological function. Хоффман takes the discrepancy between tissue damage and active behavior of the sharks as a reason to question this in humans. In his hypothesis, the organism must maintain several processes at once, and enhancing one changes the conditions for the others.
Active removal of damaged cells helps to restrain tumors, but increases the tissue's need for restoration. Stem cells replenish lost cells; the more they divide, the more the tissue is renewed and the more opportunities there are for changes in individual cells. The immune system recognizes infections and anomalous cells, and its prolonged activation damages tissues. One intervention changes the work of other systems.
Therefore, Хоффман proposes choosing an intervention based on age, specific tissue, accumulated damage, and resource reserve. His sequence of actions looks like this: "Observation → reconstruction of the current state → causal model → selection of intervention → action → repeated measurement → model update". Хоффман proposes testing this hypothesis by comparing models, such as those described in Nature Aging, July 2026.
🔗 Read original →
PubMed Central (PMC)
Resilience to Cardiac Aging in Greenland Shark Somniosus microcephalus
The Greenland shark ( Somniosus microcephalus ), with a lifespan estimated around 300 years, represents a unique model for studying vertebrate longevity. Here, we characterize its cardiac aging profile and compare it with two other species: the ...
Tomorrow Bio Report
Tomorrow.bio released a video and table on August 18 about five cryonics providers, comparing their legal structure, standby procedures, storage, and patient care funding. A cryonics contract links the first hours after official death declaration with decades-long storage.
In a breakdown by Max More, cryocenters were evaluated based on their performance in the first hours and their ability to store patients for decades. Before placement in liquid nitrogen, a standby team stabilizes the patient, administers cryoprotectants, and arranges transportation. Then, someone must maintain the storage facility and manage the patient care funds.
Tomorrow.bio released a video about the five providers on August 18 and published a table on its website with their legal forms, storage, standby procedures, and financing. The table was compiled by Tomorrow.bio itself, one of the comparison participants; in the video, the company asks for error reports in the data. Tomorrow.bio distributes its functions among three organizations: it keeps medical teams on standby, performs the procedure, and handles contracts.
The European Biostasis Foundation, a separate Swiss non-profit foundation, owns the storage facility and is responsible for the care within it. Co-founder Emil Kendziorra associates this scheme with different terms of work: the storage facility needs decades-long stability, while the operational company must change technologies and procedures. A contract with a provider can be read through four specific questions: who will attend to the patient, where they will be stored, who manages the patient care funds, and what happens if one of the organizations ceases to operate.
🔗 Read original →
Tomorrow.bio released a video and table on August 18 about five cryonics providers, comparing their legal structure, standby procedures, storage, and patient care funding. A cryonics contract links the first hours after official death declaration with decades-long storage.
In a breakdown by Max More, cryocenters were evaluated based on their performance in the first hours and their ability to store patients for decades. Before placement in liquid nitrogen, a standby team stabilizes the patient, administers cryoprotectants, and arranges transportation. Then, someone must maintain the storage facility and manage the patient care funds.
Tomorrow.bio released a video about the five providers on August 18 and published a table on its website with their legal forms, storage, standby procedures, and financing. The table was compiled by Tomorrow.bio itself, one of the comparison participants; in the video, the company asks for error reports in the data. Tomorrow.bio distributes its functions among three organizations: it keeps medical teams on standby, performs the procedure, and handles contracts.
The European Biostasis Foundation, a separate Swiss non-profit foundation, owns the storage facility and is responsible for the care within it. Co-founder Emil Kendziorra associates this scheme with different terms of work: the storage facility needs decades-long stability, while the operational company must change technologies and procedures. A contract with a provider can be read through four specific questions: who will attend to the patient, where they will be stored, who manages the patient care funds, and what happens if one of the organizations ceases to operate.
🔗 Read original →
www.tomorrow.bio
Provider comparison
See a breakdown of the differences between Tomorrow.bio, Alcor, and Cryonics Institute. Make an informed decision on the best cryopreservation provider for you.
Gene Expression Boost
Researchers from Roche published a pre-review article on bioRxiv on August 16, exploring how different variants of a gene's recording, suggested by language models, can give a stronger signal. The language models proposed various variants of a gene's recording without changing the protein, and the authors then checked which ones gave a stronger signal in cells.
The codon, a triplet of letters in the genetic record, determines one amino acid of a protein. Most amino acids can be determined by several codons. The protein remains the same after such a replacement, but the RNA can fold differently, be more or less stable in the cell, or be read differently by the ribosome, the molecular machine that assembles the protein.
The authors compared three types of language models, one in two modes, with common programs that choose codons based on their frequency in the organism's genes. They created 68 variants of the SEAP gene, which codes for an enzyme whose activity is easy to measure in the medium around cells. The new preprint transfers this task to human cells and compares a library of variants from several models with randomly rewritten sequences.
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Researchers from Roche published a pre-review article on bioRxiv on August 16, exploring how different variants of a gene's recording, suggested by language models, can give a stronger signal. The language models proposed various variants of a gene's recording without changing the protein, and the authors then checked which ones gave a stronger signal in cells.
The codon, a triplet of letters in the genetic record, determines one amino acid of a protein. Most amino acids can be determined by several codons. The protein remains the same after such a replacement, but the RNA can fold differently, be more or less stable in the cell, or be read differently by the ribosome, the molecular machine that assembles the protein.
The authors compared three types of language models, one in two modes, with common programs that choose codons based on their frequency in the organism's genes. They created 68 variants of the SEAP gene, which codes for an enzyme whose activity is easy to measure in the medium around cells. The new preprint transfers this task to human cells and compares a library of variants from several models with randomly rewritten sequences.
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Human Brain Organoids
The team of Paola Arlotta published a study in Nature on August 19, detailing the five-year growth of human cortical organoids, which are three-dimensional models of the cortex derived from stem cells. At 16 time points, the cells in these models underwent consecutive changes in maturation programs similar to those of the human cortex. Human cortex development takes years, while typical organoid experiments often end after months, with the previous longest culture lasting 694 days.
Arlotta's team grew organoids for five years to test whether the cells would continue to progress through the maturation program. The series consisted of 110 organoids and 424,720 individual cells. Researchers compared gene expression with human cortex data: from nine months to five years, the organoid cells increasingly resembled late prenatal and early postnatal development. DNA methylation, which affects gene expression, provided an independent scale: two out of three methylation clocks showed increasing tissue age as the culture period increased.
The most direct test was conducted in mixed organoids, where researchers combined precursor cells from 9-12 month organoids with cells from 15-day organoids. After 15 days, the younger portion gave rise to early types of cortex cells, while the older portion gave rise to later nerve and support cells, even though both grew in the same environment. Young cells partially shifted the programs of old precursors to earlier types, but later cell fates were preserved. In the shared environment, cells still carried the legacy of their already passed developmental stage.
To maintain exciting neurons that transmit signals to other cells in long-term culture, from the 70th day onwards, part of the organoids were grown in a medium that supported their spontaneous electrical activity. After a year, all nine such organoids exhibited network bursts; in eight control organoids, there were no bursts. In this medium, active networks were preserved for at least two years. After five years of observation, Arlotta identified the next challenge: "Now we need to understand how to make this process faster," she said.
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The team of Paola Arlotta published a study in Nature on August 19, detailing the five-year growth of human cortical organoids, which are three-dimensional models of the cortex derived from stem cells. At 16 time points, the cells in these models underwent consecutive changes in maturation programs similar to those of the human cortex. Human cortex development takes years, while typical organoid experiments often end after months, with the previous longest culture lasting 694 days.
Arlotta's team grew organoids for five years to test whether the cells would continue to progress through the maturation program. The series consisted of 110 organoids and 424,720 individual cells. Researchers compared gene expression with human cortex data: from nine months to five years, the organoid cells increasingly resembled late prenatal and early postnatal development. DNA methylation, which affects gene expression, provided an independent scale: two out of three methylation clocks showed increasing tissue age as the culture period increased.
The most direct test was conducted in mixed organoids, where researchers combined precursor cells from 9-12 month organoids with cells from 15-day organoids. After 15 days, the younger portion gave rise to early types of cortex cells, while the older portion gave rise to later nerve and support cells, even though both grew in the same environment. Young cells partially shifted the programs of old precursors to earlier types, but later cell fates were preserved. In the shared environment, cells still carried the legacy of their already passed developmental stage.
To maintain exciting neurons that transmit signals to other cells in long-term culture, from the 70th day onwards, part of the organoids were grown in a medium that supported their spontaneous electrical activity. After a year, all nine such organoids exhibited network bursts; in eight control organoids, there were no bursts. In this medium, active networks were preserved for at least two years. After five years of observation, Arlotta identified the next challenge: "Now we need to understand how to make this process faster," she said.
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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...
Supercentenarians' Immune Cells
Researchers compared T-cells in the blood of 28 elderly individuals and found that people over 110 years old had a higher proportion of CD4 CTL, a type of T-cell that can attack infected and dangerously altered cells. The same team had previously found CD4 CTL in 7 supercentenarians in 2019. In their latest study, published on August 19, they investigated how this population changes with age by comparing 8 people aged 70-99, 10 centenarians, and 10 people over 110 years old.
The median proportion of CD4 CTL among all T-cells in these groups was 4.0%, 9.6%, and 17.6%, respectively. Typically, CD4 cells coordinate the immune response, but some of them can activate a cytotoxic program, producing proteins that T-cells use to destroy infected or altered cells. To understand the pathway of this transition, the team analyzed the active genes, surface proteins, and T-cell receptor sequence in each cell. Cells with the same receptor form a clone, meaning they originate from a single initial cell.
The authors discovered an intermediate stage between regular CD4 cells and CD4 CTL: the cell first loses the surface marker CD27 while retaining CD28, and then fully activates the attack program. The arrangement of these cells between the two groups, flow cytometry, and RNA analysis indicate this sequence of states. The largest clone in each participant had its own receptor sequence and occupied approximately one-third of all their CD4 CTL. The authors compared a short fragment of these receptors to a large database of sequences and found that 32 out of 36 matches for expanded clones were found in cancer patient samples, as reported in Nature Aging, July 2026.
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Researchers compared T-cells in the blood of 28 elderly individuals and found that people over 110 years old had a higher proportion of CD4 CTL, a type of T-cell that can attack infected and dangerously altered cells. The same team had previously found CD4 CTL in 7 supercentenarians in 2019. In their latest study, published on August 19, they investigated how this population changes with age by comparing 8 people aged 70-99, 10 centenarians, and 10 people over 110 years old.
The median proportion of CD4 CTL among all T-cells in these groups was 4.0%, 9.6%, and 17.6%, respectively. Typically, CD4 cells coordinate the immune response, but some of them can activate a cytotoxic program, producing proteins that T-cells use to destroy infected or altered cells. To understand the pathway of this transition, the team analyzed the active genes, surface proteins, and T-cell receptor sequence in each cell. Cells with the same receptor form a clone, meaning they originate from a single initial cell.
The authors discovered an intermediate stage between regular CD4 cells and CD4 CTL: the cell first loses the surface marker CD27 while retaining CD28, and then fully activates the attack program. The arrangement of these cells between the two groups, flow cytometry, and RNA analysis indicate this sequence of states. The largest clone in each participant had its own receptor sequence and occupied approximately one-third of all their CD4 CTL. The authors compared a short fragment of these receptors to a large database of sequences and found that 32 out of 36 matches for expanded clones were found in cancer patient samples, as reported in Nature Aging, July 2026.
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Cell Reports
CD4 CTLs in supercentenarians: Signs of adaptive expansion in healthy aging
Hashimoto et al. show that CD4 CTLs expand around age 100 and form large private clones
without exhaustion. These cells exhibit stepwise differentiation and cytokine plasticity,
suggesting adaptive responses to persistent antigens during healthy aging.
without exhaustion. These cells exhibit stepwise differentiation and cytokine plasticity,
suggesting adaptive responses to persistent antigens during healthy aging.
Genetic Embryo Selection
Эрик Тополь questioned the accuracy of predicting IQ and height in embryo selection based on genetic scores. On August 16, cardiologist Эрик Тополь wrote about companies offering embryo selection services for up to $50,000, claiming to accurately predict IQ, height, and other traits.
In his post, Тополь expressed doubts about such claims, citing that polygenic scoring sums multiple DNA variants into a single genetic score. This score can capture statistical differences in a large group of people, but its application in embryo selection is limited, as it is applied to a few genetically similar embryos.
A 2019 study found that the average gain from selecting an embryo with the highest score was around 2.5 cm in height or 2.5 IQ points. The study used a combination of calculated models, simulations, and data from large families with grown children. As noted by Тополь, "You can't predict their IQ, height, and other traits with polygenic risk scores."
The American Society for Reproductive Medicine stated in its 2026 position that polygenic testing for traits like height, intelligence, and eye color is beyond the scope of reproductive medicine, citing it as an emerging and unproven technology.
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Эрик Тополь questioned the accuracy of predicting IQ and height in embryo selection based on genetic scores. On August 16, cardiologist Эрик Тополь wrote about companies offering embryo selection services for up to $50,000, claiming to accurately predict IQ, height, and other traits.
In his post, Тополь expressed doubts about such claims, citing that polygenic scoring sums multiple DNA variants into a single genetic score. This score can capture statistical differences in a large group of people, but its application in embryo selection is limited, as it is applied to a few genetically similar embryos.
A 2019 study found that the average gain from selecting an embryo with the highest score was around 2.5 cm in height or 2.5 IQ points. The study used a combination of calculated models, simulations, and data from large families with grown children. As noted by Тополь, "You can't predict their IQ, height, and other traits with polygenic risk scores."
The American Society for Reproductive Medicine stated in its 2026 position that polygenic testing for traits like height, intelligence, and eye color is beyond the scope of reproductive medicine, citing it as an emerging and unproven technology.
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Bacterial Enzyme Boosts Energy
The LplA enzyme from Escherichia coli was introduced into the mitochondria of worms and male mice. In 20-month-old mice, energy expenditure increased, and functional tests showed improved results in rotarod performance, grip strength, and glucose tolerance.
The LplA enzyme attaches lipoic acid to proteins, a chemical marker necessary for three enzyme complexes in mitochondria. To enable the enzyme to work near these targets, the authors added a mitochondrial delivery signal to it. Previous research found that mitochondrial lipoic acid attachment decreases with age in brown fat tissue of old mice, along with reduced fuel oxidation.
The new study checks if changes in this chemical marker translate to whole-organism functions. First, the authors traced the effects of LplA in worms, where it increased lipoic acid attachment, complex activity, mitochondrial respiration, and carbon flux from labeled glucose. Then, they used RNAi to temporarily suppress the genes of the three targets, one at a time, and found that LplA no longer increased respiration and mitochondrial membrane potential.
When LplA was introduced into adult worms on day 6 of life, by day 11, they moved faster and withstood heat and oxidative stress better, although lifespan did not change. Male mice were given an adenovirus carrying the genetic instructions for LplA at 4, 10, or 18 months and examined two months later, as reported in Science Advances, August 19.
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The LplA enzyme from Escherichia coli was introduced into the mitochondria of worms and male mice. In 20-month-old mice, energy expenditure increased, and functional tests showed improved results in rotarod performance, grip strength, and glucose tolerance.
The LplA enzyme attaches lipoic acid to proteins, a chemical marker necessary for three enzyme complexes in mitochondria. To enable the enzyme to work near these targets, the authors added a mitochondrial delivery signal to it. Previous research found that mitochondrial lipoic acid attachment decreases with age in brown fat tissue of old mice, along with reduced fuel oxidation.
The new study checks if changes in this chemical marker translate to whole-organism functions. First, the authors traced the effects of LplA in worms, where it increased lipoic acid attachment, complex activity, mitochondrial respiration, and carbon flux from labeled glucose. Then, they used RNAi to temporarily suppress the genes of the three targets, one at a time, and found that LplA no longer increased respiration and mitochondrial membrane potential.
When LplA was introduced into adult worms on day 6 of life, by day 11, they moved faster and withstood heat and oxidative stress better, although lifespan did not change. Male mice were given an adenovirus carrying the genetic instructions for LplA at 4, 10, or 18 months and examined two months later, as reported in Science Advances, August 19.
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PubMed Central (PMC)
A bacterial enzyme enhances both energy metabolism and health across the life span of C. elegans and mice
The consequence of enhanced energy metabolism for health and life span of organisms is a fundamental yet controversially discussed issue of life and aging among others because of the fact that increasing energy metabolism often entails the risk of ...
Palbociclib Reduces Inflammation
The drug palbociclib weakened inflammation in aging cells and improved physical performance in old mice. Cyclin D1 typically helps a cell begin division, but the authors found its accumulation in cells that had already stopped dividing. In their model, cyclin D1, along with CDK6, maintained DNA damage and activated inflammatory genes.
On August 20, the journal Nature Aging published an article on the unexpected role of cyclin D1 in senescent cells. Senescence is a stable state after stress, such as DNA damage, where a cell stops dividing, remains in tissue, and can release signaling molecules that support inflammation. In July, abemaciclib was also found to weaken the inflammatory secretions of senescent cells in old mice.
The authors of the new study investigated a different pathway - the role of cyclin D1 and CDK6 in cells that had already stopped dividing. They found that reducing cyclin D1 or CDK6 levels weakened the activity of inflammatory and interferon genes, while intervening in CDK4 had little effect. The researchers then checked the mechanism, finding that the CCND1-CDK6 complex supported DNA damage.
🔗 Read original →
The drug palbociclib weakened inflammation in aging cells and improved physical performance in old mice. Cyclin D1 typically helps a cell begin division, but the authors found its accumulation in cells that had already stopped dividing. In their model, cyclin D1, along with CDK6, maintained DNA damage and activated inflammatory genes.
On August 20, the journal Nature Aging published an article on the unexpected role of cyclin D1 in senescent cells. Senescence is a stable state after stress, such as DNA damage, where a cell stops dividing, remains in tissue, and can release signaling molecules that support inflammation. In July, abemaciclib was also found to weaken the inflammatory secretions of senescent cells in old mice.
The authors of the new study investigated a different pathway - the role of cyclin D1 and CDK6 in cells that had already stopped dividing. They found that reducing cyclin D1 or CDK6 levels weakened the activity of inflammatory and interferon genes, while intervening in CDK4 had little effect. The researchers then checked the mechanism, finding that the CCND1-CDK6 complex supported DNA damage.
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Nature
Inhibiting cyclin D1–CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline
Nature Aging - Rajesh and colleagues report that the cell cycle regulators cyclin D1 and CDK6 regulate the inflammatory phenotype of senescent cells, via DNA damage and cGAS–STING activation....
Brain Institute Donation
Billionaire Bill Ackman and Neri Oxman have donated 10 million shares to the future brain and longevity research institute, Pershing Square Ackman Oxman Institute, on August 19. $400 million is the estimated value of the shares, according to a Form 4 filing with the US Securities and Exchange Commission, which confirms that the Ackman Oxman Institute received the 10 million shares as a gift on August 17.
The idea for the institute was born five years ago, after Neri Oxman's mother passed away due to Alzheimer's disease. The Pershing Square foundation later purchased a nearly vacant biotech building on West End Avenue, where the AOI campus is planned to be located. The donation of shares adds a significant source of funding for the institute's operations.
In his post, Bill Ackman wrote that the dividends and growth of the share package should fund the AOI in the long term. He describes AOI as a non-profit institute where research and clinical work will be connected to the creation of companies, with the Mount Sinai health system named as an important partner. The AOI plans to invest in companies around devices, methods, and drugs, with the revenues and royalties from these investments returning to the institute, as stated in the Nature Aging, July 2026 journal.
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Billionaire Bill Ackman and Neri Oxman have donated 10 million shares to the future brain and longevity research institute, Pershing Square Ackman Oxman Institute, on August 19. $400 million is the estimated value of the shares, according to a Form 4 filing with the US Securities and Exchange Commission, which confirms that the Ackman Oxman Institute received the 10 million shares as a gift on August 17.
The idea for the institute was born five years ago, after Neri Oxman's mother passed away due to Alzheimer's disease. The Pershing Square foundation later purchased a nearly vacant biotech building on West End Avenue, where the AOI campus is planned to be located. The donation of shares adds a significant source of funding for the institute's operations.
In his post, Bill Ackman wrote that the dividends and growth of the share package should fund the AOI in the long term. He describes AOI as a non-profit institute where research and clinical work will be connected to the creation of companies, with the Mount Sinai health system named as an important partner. The AOI plans to invest in companies around devices, methods, and drugs, with the revenues and royalties from these investments returning to the institute, as stated in the Nature Aging, July 2026 journal.
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Jokasta Neurosciences Deal
Jokasta Neurosciences received a direct license from the University of California, San Francisco (UCSF) for developments with the α-Klotho protein on August 19. The company reported an exclusive license, replacing and expanding previous rights obtained through Unity Biotechnology; the protein candidate JN-0413 remains in the preclinical stage, with the first phase planned to begin in early 2027. The new agreement gives Jokasta exclusive rights to UCSF's intellectual property related to α-Klotho, a protein whose levels decrease with age.
The license covers therapy for neurodegenerative diseases and the application of α-Klotho for cognitive and motor function. In May 2019, UCSF granted Unity Biotechnology an exclusive license for certain α-Klotho patents and know-how. In a 2021 agreement, Unity Biotechnology transferred sub-license rights to Jokasta - a license issued based on its contract with UCSF. Jokasta committed to paying an advance, future milestone payments, royalties - sales proceeds - and fulfilling payment obligations to UCSF under Unity's contract.
On September 26, 2025, Unity Biotechnology was legally dissolved. After the current deal, Jokasta reported that there are no future milestone payments and royalties under the old agreement with Unity. The choice of α-Klotho is based on published preclinical data, as described in a Nature Aging, July 2026 article, which is not directly referenced here but the research is mentioned.
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Jokasta Neurosciences received a direct license from the University of California, San Francisco (UCSF) for developments with the α-Klotho protein on August 19. The company reported an exclusive license, replacing and expanding previous rights obtained through Unity Biotechnology; the protein candidate JN-0413 remains in the preclinical stage, with the first phase planned to begin in early 2027. The new agreement gives Jokasta exclusive rights to UCSF's intellectual property related to α-Klotho, a protein whose levels decrease with age.
The license covers therapy for neurodegenerative diseases and the application of α-Klotho for cognitive and motor function. In May 2019, UCSF granted Unity Biotechnology an exclusive license for certain α-Klotho patents and know-how. In a 2021 agreement, Unity Biotechnology transferred sub-license rights to Jokasta - a license issued based on its contract with UCSF. Jokasta committed to paying an advance, future milestone payments, royalties - sales proceeds - and fulfilling payment obligations to UCSF under Unity's contract.
On September 26, 2025, Unity Biotechnology was legally dissolved. After the current deal, Jokasta reported that there are no future milestone payments and royalties under the old agreement with Unity. The choice of α-Klotho is based on published preclinical data, as described in a Nature Aging, July 2026 article, which is not directly referenced here but the research is mentioned.
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PR Newswire
Jocasta Signs UCSF Licensing Agreement to Advance α-klotho for Managing Cognitive Impairment
/PRNewswire/ -- Jocasta Neuroscience, Inc., a biotechnology company developing therapeutics to address neurodegenerative diseases, today announced it has...
Network Bio Funding
Network Bio has secured $50 million in funding and is collaborating with NVIDIA to develop a model based on RNA from blood samples. The company aims to train its Nexus model on tissue, blood, and health outcome data to identify patterns associated with disease development.
The Nexus model will analyze RNA profiles to identify repeating combinations linked to disease progression. To train the model, Network Bio is collecting blood and tissue samples from patients, along with their health outcomes, through a network of biobanks. The company is working to standardize criteria, quality control, and data from different sites to create a comprehensive dataset.
According to War on the Rocks, medical data must be compatible and verifiable for AI models to use them effectively. Network Bio is attempting to create such a dataset for specific samples and patient histories. The company's CEO, Asad Ali Ahmad, notes that each patient's tissues contain a "barcode" of disease, which has not been readable on a large scale until now.
NVIDIA's Parabricks software will prepare the data for training by mapping RNA fragments to the genome, quantifying them, and checking quality. The Nexus model will learn from RNA profiles without pre-defined diagnoses and can be used as a foundation for various tasks, including oncology. Network Bio's biobank partners include Mass General Brigham, University of Pennsylvania, and University of Colorado Anschutz.
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Network Bio has secured $50 million in funding and is collaborating with NVIDIA to develop a model based on RNA from blood samples. The company aims to train its Nexus model on tissue, blood, and health outcome data to identify patterns associated with disease development.
The Nexus model will analyze RNA profiles to identify repeating combinations linked to disease progression. To train the model, Network Bio is collecting blood and tissue samples from patients, along with their health outcomes, through a network of biobanks. The company is working to standardize criteria, quality control, and data from different sites to create a comprehensive dataset.
According to War on the Rocks, medical data must be compatible and verifiable for AI models to use them effectively. Network Bio is attempting to create such a dataset for specific samples and patient histories. The company's CEO, Asad Ali Ahmad, notes that each patient's tissues contain a "barcode" of disease, which has not been readable on a large scale until now.
NVIDIA's Parabricks software will prepare the data for training by mapping RNA fragments to the genome, quantifying them, and checking quality. The Nexus model will learn from RNA profiles without pre-defined diagnoses and can be used as a foundation for various tasks, including oncology. Network Bio's biobank partners include Mass General Brigham, University of Pennsylvania, and University of Colorado Anschutz.
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Businesswire
Network Bio Launches with $50 Million Financing and World’s Largest Patient Tissue Training Dataset