Lifespan Research Institute Launches Public Longevity Group

Date Posted: September 17, 2025

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Lifespan Research Institute Launches Public Longevity Group

[Mountain View, September 17, 2025] — Lifespan Research Institute (LRI) today announced the launch of the Public Longevity Group (PLG), a new initiative focused on bridging the cultural gap between scientific breakthroughs in aging and their public acceptance. To kickstart its work, PLG has opened a crowdfunding campaign to develop tools that measure and strengthen public trust in longevity science.

While the science of longevity biotechnology continues to advance, skepticism and cultural resistance limit progress, with some studies showing that more than half of Americans would reject a safe, proven therapy to extend life. This hesitation poses risks of raising costs, delaying health-promoting regulation, and slowing the delivery of treatments that could combat age-related diseases and extend healthy lifespan.

“The breakthrough that unlocks all other breakthroughs is public trust,” said Sho Joseph Ozaki Tan, Founder of PLG. “Without it, even the most promising therapies may never reach the people they’re meant to help. PLG exists to change that.”

“Persuasion is a science too,” said Keith Comito, CEO of Lifespan Research Institute. “To bring health-extending technologies to the public as quickly as possible, we must approach advocacy with the same rigor as our research. With PLG, we’ll be able to systematically measure and increase social receptivity, making the public’s appetite for credible longevity therapies unmistakable to policymakers, investors, and the public itself.”

PLG is developing the first data-driven cultural intelligence system for longevity—a platform designed to track real-time sentiment, test narratives, and identify which messages resonate and which backfire. Early tools include:

The Longevity Cultural Clock: a cultural barometer mapping readiness and resistance across demographics and regions.
Sentiment Dashboards: real-time monitoring of public, investor, and policymaker perceptions.
Narrative Testing Tools: data-driven analysis that will enable robust pathways to public support.

The crowdfunding campaign will provide the initial $100,000 needed to launch these tools, creating the cultural foundation required for healthier, longer lives.

With a lean, data-driven team, the group aims to provide open-access cultural insights for advocates and policymakers while offering advanced analytics to mission-aligned partners.

Campaign Timeline:

Campaign completion: November 2, 2025
Dashboard development: Dec 2025 – Feb 2026
First survey deployment: Feb – Apr 2026
Beta dashboard launch: May 2026
First public insight report: June 2026

Supporters can contribute directly at: https://lifespan.io/campaigns/public-longevity-group/

The PLG campaign is sponsored by the members of LRI’s Lifespan Alliance, a consortium of mission-aligned organizations that believe in the promise of extending healthy human lifespan. Newly-joined members include OpenCures, AgelessRx, and Lento Bio.

About Lifespan Research Institute

Lifespan Research Institute accelerates the science and systems needed for longer, healthier lives by uniting researchers, investors, and the public to drive lasting impact. LRI advances breakthrough science, builds high-impact ecosystems, and connects the global longevity community.

Media Contact:

Christie Sacco

Marketing Director

Lifespan Research Institute

christie.sacco@lifespan.io

(650) 336-1780

We would like to ask you a small favor. We are a non-profit foundation, and unlike some other organizations, we have no shareholders and no products to sell you. All our news and educational content is free for everyone to read, but it does mean that we rely on the help of people like you. Every contribution, no matter if it’s big or small, supports independent ethical journalism and sustains our future.

Yes I will donate❤️

Date Posted: September 23, 2026

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Physical Activity Delays Ovarian Aging in Mice

Results from a recent study suggest a delay in ovarian aging in mice following treadmill training; this effect was mediated by adiponectin. Pharmacologically activating adiponectin receptors extended reproductive span in mice. [1]

Beyond reproduction

The female reproductive system strongly influences the female aging trajectory, and its impact goes well beyond the cessation of reproduction. While ovarian aging is accompanied by a decline in the ability to produce egg cells capable of fertilization and a healthy pregnancy (ovarian reserve), it also spurs hormonal changes that affect the brain, bones, muscles, cardiovascular system, mental health, and more [2, 3].

Given that about half of the population undergoes ovarian aging, interventions are needed to slow it down. So far, the only available option, hormone replacement therapy, can be used to alleviate symptoms of menopausal transition, but it’s unable to prevent ovarian aging.

Exercise and ovarian reserve

One intervention known to slow aging in other organs, such as the brain or skeletal muscle, is physical activity [4]; however, whether physical activity affects ovarian aging is still debated, as studies so far have produced mixed results [5-8].

The authors of this study analyzed data from over 150,000 women across two studies and found that postmenopausal women have lower physical activity levels than premenopausal women. While these differences might stem from other factors, the authors suggested that ovarian aging might be implicated.

To test the impact of physical activity on ovarian aging, they used adult female mice that underwent 1 month of treadmill exercise training. Comparing this group with mice that didn’t exercise showed that exercise can help preserve ovarian reserve in adult mice and reduce primordial follicle loss. Primordial follicles contain an immature oocyte arrested in early development. Each female has a set number of follicles at birth, and, over time, those reserves are depleted because, in each menstrual cycle, several are recruited and one develops into a mature oocyte ready for fertilization.

Mice in the exercise group had more primordial follicles than controls. The exercise group also had higher AMH, an ovarian reserve marker, and increased levels of growth factors produced by oocytes.

The mediator of the effect

One molecule previously reported to increase with exercise is adiponectin [9], a hormone mainly produced by fat tissue that positively affects metabolism (e.g., insulin sensitivity) and reduces inflammation. It has also been reported to extend lifespan in mice [9] and slow muscle and brain aging [10, 11]. Adiponectin expression is also reduced in aging ovaries of model animals [12].

Those researchers hypothesize that adiponectin mediates exercise’s protective impact on ovarian health and delays ovarian aging. Their results supported this hypothesis and showed higher adiponectin levels in the exercise group than in the control group.

Adiponectin has previously been shown to regulate the mTOR signaling pathway [13]. Moreover, one mTOR pathway component was suggested as the primary activator of primordial follicle development [14]. In this study, the researchers observed lower levels of phosphorylated mTOR (p-mTOR) and phosphorylated rpS6 (p-rpS6) in the exercise group than in the control group, suggesting reduced mTOR signaling.

To investigate this further, they tested cultured newborn mouse ovaries exposed to various adiponectin levels. Higher adiponectin significantly reduced the proportion of growing follicles and p-mTOR levels compared with the control group. Decreased adiponectin levels resulted in more growing follicles and higher mTOR levels. These data suggest that “adiponectin regulates follicle activation through suppression of the mTOR signaling pathway.”

Further investigation found that adiponectin-deficient mice have fewer follicles than wild-type mice. After exercise, the number of follicles in wild-type and adiponectin-deficient mice was higher than in the non-exercised groups, but the protective effect of exercise was significantly less pronounced in adiponectin-deficient mice.

While adiponectin is mainly produced by adipose tissue, some adiponectin is also produced by ovaries. The protective role of exercise was significantly reduced against primordial follicle loss in mice with ovary-specific adiponectin knockout (76% reduction compared to wild-type). Additionally, the ovary-specific adiponectin-knockdown exercise group had reduced mTOR protein phosphorylation in the ovaries compared with controls, suggesting that ovarian adiponectin plays a significant role in how exercise delays ovarian aging.

An exercise substitute

After identifying the molecules mediating exercise’s effect on ovarian aging, the researchers looked for molecules that could affect those pathways. They identified AdipoRon, an adiponectin receptor agonist that binds to and activates the adiponectin receptor, as a good candidate to substitute for exercise to delay ovarian aging.

Adult mice received AdipoRon for one month. The treatment group had significantly more primordial follicles, more total follicles, higher AMH protein levels, and higher adiponectin receptor 1 protein levels within the ovaries than the control group, but adiponectin levels did not differ significantly between groups. Additionally, p-mTOR and p-rpS6 protein levels in the ovaries were lower in the AdipoRon-treated group. Similar results were obtained when mice were treated at their mid-reproductive age. These effects persisted for a few months, which is already an older age in mice.

The reproductive capacity of female mice also improved following AdipoRon treatment. While AdipoRon-treated females at mid-reproductive age had a similar number of offspring as control mice, as mice aged, AdipoRon-treated females had significantly more offspring than the untreated group. At an age when control animals had almost stopped producing offspring, most AdipoRon-treated mice were still producing offspring.

The authors conclude that both physical activity “and adiponectin may serve as promising targets for delaying ovarian aging, with substantial implications for both reproductive health and longevity.”

Yes I will donate❤️

Literature

[1] Li, B., Zheng, N., Luo, T., Chen, Y., Mei, X., Huang, Q., Wang, W., Li, L., Han, L., Wang, W., Lin, B., Fan, Y., Liu, Y., Liu, Z., Ai, S., Liang, Y. Y., Wang, H., Tan, X., Zhang, M., Feng, H., … Zhang, J. (2026). Physical activity delays ovarian aging in part through adiponectin-related signaling pathways. Nature aging, 6(9), 1886–1900.

[2] Coughlan, G. T., Betthauser, T. J., Boyle, R., Koscik, R. L., Klinger, H. M., Chibnik, L. B., Jonaitis, E. M., Yau, W. W., Wenzel, A., Christian, B. T., Gleason, C. E., Saelzler, U. G., Properzi, M. J., Schultz, A. P., Hanseeuw, B. J., Manson, J. E., Rentz, D. M., Johnson, K. A., Sperling, R., Johnson, S. C., … Buckley, R. F. (2023). Association of Age at Menopause and Hormone Therapy Use With Tau and β-Amyloid Positron Emission Tomography. JAMA neurology, 80(5), 462–473.

[3] Mehta, J. M., & Manson, J. E. (2024). The menopausal transition period and cardiovascular risk. Nature reviews. Cardiology, 21(3), 203–211.

[4] Sun, S., Ma, S., Cai, Y., Wang, S., Ren, J., Yang, Y., Ping, J., Wang, X., Zhang, Y., Yan, H., Li, W., Esteban, C. R., Yu, Y., Liu, F., Izpisua Belmonte, J. C., Zhang, W., Qu, J., & Liu, G. H. (2023). A single-cell transcriptomic atlas of exercise-induced anti-inflammatory and geroprotective effects across the body. Innovation (Cambridge (Mass.)), 4(1), 100380.

[5] Zhao, M., Whitcomb, B. W., Purdue-Smithe, A. C., Manson, J. E., Hankinson, S. E., Rosner, B. A., & Bertone-Johnson, E. R. (2018). Physical activity is not related to risk of early menopause in a large prospective study. Human reproduction (Oxford, England), 33(10), 1960–1967.

[6] Kiranmayee, D., Praveena, T., Himabindu, Y., Sriharibabu, M., Kavya, K., & Mahalakshmi, M. (2017). The Effect of Moderate Physical Activity on Ovarian Reserve Markers in Reproductive Age Women Below and Above 30 Years. Journal of human reproductive sciences, 10(1), 44–48.

[7] Gudmundsdottir, S. L., Flanders, W. D., & Augestad, L. B. (2013). Physical activity and age at menopause: the Nord-Trøndelag population-based health study. Climacteric : the journal of the International Menopause Society, 16(1), 78–87.

[8] Dorjgochoo, T., Kallianpur, A., Gao, Y. T., Cai, H., Yang, G., Li, H., Zheng, W., & Shu, X. O. (2008). Dietary and lifestyle predictors of age at natural menopause and reproductive span in the Shanghai Women’s Health Study. Menopause (New York, N.Y.), 15(5), 924–933.

[9] Liu, L., Tang, J., Liang, X., Li, Y., Zhu, P., Zhou, M., Qin, L., Deng, Y., Li, J., Wang, Y., Jiang, L., Huang, D., Zhou, Y., Wang, S., Xiao, Q., Luo, Y., & Tang, Y. (2024). Running exercise alleviates hippocampal neuroinflammation and shifts the balance of microglial M1/M2 polarization through adiponectin/AdipoR1 pathway activation in mice exposed to chronic unpredictable stress. Molecular psychiatry, 29(7), 2031–2042.

[10] Selvais, C. M., Davis-López de Carrizosa, M. A., Nachit, M., Versele, R., Dubuisson, N., Noel, L., Gillard, J., Leclercq, I. A., Brichard, S. M., & Abou-Samra, M. (2023). AdipoRon enhances healthspan in middle-aged obese mice: striking alleviation of myosteatosis and muscle degenerative markers. Journal of cachexia, sarcopenia and muscle, 14(1), 464–478.

[11] He, K., Nie, L., Ali, T., Liu, Z., Li, W., Gao, R., Zhang, Z., Liu, J., Dai, Z., Xie, Y., Zhang, Z., Liu, G., Dong, M., Yu, Z. J., Li, S., & Yang, X. (2023). Adiponectin deficiency accelerates brain aging via mitochondria-associated neuroinflammation. Immunity & ageing : I & A, 20(1), 15.

[12] Wu, M., Huang, Y., Zhu, Q., Zhu, X., Xue, L., Xiong, J., Chen, Y., Wu, C., Guo, Y., Li, Y., Wu, M., & Wang, S. (2022). Adipose tissue and ovarian aging: Potential mechanism and protective strategies. Ageing research reviews, 80, 101683.

[13] Park, J. S., Choe, K., Lee, H. J., Park, T. J., & Kim, M. O. (2023). Neuroprotective effects of osmotin in Parkinson’s disease-associated pathology via the AdipoR1/MAPK/AMPK/mTOR signaling pathways. Journal of biomedical science, 30(1), 66.

[14] Zhang, H., Risal, S., Gorre, N., Busayavalasa, K., Li, X., Shen, Y., Bosbach, B., Brännström, M., & Liu, K. (2014). Somatic cells initiate primordial follicle activation and govern the development of dormant oocytes in mice. Current biology : CB, 24(21), 2501–2508.

Date Posted: September 22, 2026

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Transplanted Immune Cells Donate Mitochondria to Neighbors

According to a new study using a mouse model of a rare disease, transplanted immune cells donate their mitochondria to neighboring donor cells, improving energy production and rescuing function [1].

Here, have some mitochondria

Friedreich’s ataxia is a rare genetic disease in which deficiency in the protein frataxin impairs mitochondrial energy production, especially in energy-hungry cells such as heart muscle cells (cardiomyocytes) and neurons [2]. This causes heart disease, movement problems, and other complications typical of this disease. Mitochondrial dysfunction is also an important hallmark of aging, underlying multiple age-related conditions [3].

Microglia, the brain’s resident immune cells, and macrophages, related immune cells in other tissues, also become dysfunctional in Friedreich’s ataxia. Restoring these immune cells is possible via a bone marrow transplant.

However, there might be an additional benefit: immune cells are known to transfer their mitochondria to neighboring cells [4]. What if donor immune cells could replace diseased cells and also donate mitochondria to neighboring non-immune cells, rescuing their metabolism? This was the premise of a new study from Stanford University that was published in Nature Communications.

Mitochondrial transfer confirmed

Previous bone marrow transplantation studies had shown benefits in mouse models of Friedreich’s ataxia, but replacement of brain microglia was inefficient [5]. To solve this, the authors developed a conditioning regimen that greatly improves the replacement rate.

The researchers used YG8-800 mice, which lack the mouse frataxin gene but carry a human FXN gene with a pathogenic mutation, recapitulating several features of the disease. Before transplantation, the mice were given the drug busulfan, which depletes blood-forming cells and makes room for the graft; after transplantation, they were given pexidartinib, which depletes existing microglia, helping open the brain’s microglial niche to replacement cells.

To distinguish donor cells from donated mitochondrial material, the healthy donor marrow carried two fluorescent labels: green GFP throughout the cell and red mKate2 targeted to mitochondria.

The treatment achieved extensive donor-cell engraftment in blood and brain. Around five months after transplantation, approximately 82% of the measured brain microglial/myeloid population in affected recipients was donor-derived.

The researchers then looked for recipient cells that contained the red mitochondrial label but lacked the green donor-cell label. Recipient brain cells acquired donor mitochondrial signals, and acquisition or retention was greater in affected mice than in healthy mice.

The signal was detected across several brain cell populations, including neurons and supporting cells. This showed that donor cells were distributed widely through the brain and that this distribution was accompanied by mitochondrial transfer.

Interestingly, cells outside the brain also showed signs of mitochondrial transfer from donor cells. In bone marrow, about 22% of the remaining recipient cells were positive for the mitochondrial label.

Functional improvement

Healthy marrow improved growth and reduced hair loss in affected mice. In terms of body weight, treated mice were roughly in the middle between the untreated mice (affected mice who had received affected bone marrow) and healthy controls: the treatment recovered about half the weight deficit.

Female survival improved from about 53% in affected controls to 80% with healthy marrow. Males also showed improved growth and hair condition, but their survival improvement was nonsignificant.

The researchers then tested females at approximately 29-30 weeks, when this model shows motor abnormalities. Treated mice performed better in coordination, spontaneous movement, and strength tests, although they did not quite reach healthy levels of performance.

Transfer on contact

Single-cell RNA sequencing then revealed the mitochondrial signal across a broad range of brain cell types. Signal-positive cells showed coordinated changes in energy-metabolism genes. In these cells, many nuclear genes involved in energy production were more active. Other changes involved antioxidant defenses and cellular maintenance.

However, expression of genes encoded by mitochondrial DNA often decreased rather than increased. The authors suggest possible explanations, including normalization of compensatory responses or changes in mitochondrial quality control, but these are speculative at this point.

Proteomic analysis found that healthy marrow partially restored proteins associated with synapses. Severely depleted mitochondrial respiratory-chain proteins also recovered toward healthy levels.

As cardiac disease is a major component of Friedreich’s ataxia, the researchers then examined the heart. Donor-derived macrophages populated the heart, and donor mitochondrial signals also appeared outside donor cells. Echocardiography then showed that healthy marrow partially improved cardiac pumping performance.

To better understand the mechanism behind mitochondrial transfer, the authors cultured healthy donor macrophages together with fibroblasts from healthy or affected mice. Affected fibroblasts acquired much more mitochondrial signal than healthy fibroblasts. No transfer was detected when the cells were physically separated under the tested conditions, suggesting a contact-dependent mechanism.

The affected cells carrying donor mitochondrial signals showed a clear improvement in respiratory capacity. However, recovery remained incomplete: recipient cells performed better than affected controls but worse than healthy cells.

“It’s a way to use the blood system to treat non-blood organs,” said senior study author Natalia Gomez-Ospina, MD, Ph.D., assistant professor of pediatrics. “It’s profound. Cells are talking to each other in ways that are more consequential than we’ve realized, and this has many implications for disease treatment. For instance, the brain can say, ‘Uh oh, my microglia have been depleted. Let’s repopulate them from the bone marrow. We can leverage that process to get healthy cells into the brain.”

Yes I will donate❤️

Literature

[1] Cho, H., Sayana, R., Koladiya, A., Colella, P., Cho, S., Jahng, J. W., … & Gomez-Ospina, N. (2026). Myeloid cell replacement induces intercellular mitochondrial transfer and restores metabolism in a mouse model of mitochondrial disease. Nature Communications.

[2] Lynch, D. R., & Farmer, G. (2021). Mitochondrial and metabolic dysfunction in Friedreich ataxia: update on pathophysiological relevance and clinical interventions. Neuronal signaling, 5(2), NS20200093.

[3] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2023). Hallmarks of aging: An expanding universe. Cell, 186(2), 243-278.

[4] Scheiblich, H., Eikens, F., Wischhof, L., Opitz, S., Jüngling, K., Cserép, C., … & Heneka, M. T. (2024). Microglia rescue neurons from aggregate-induced neuronal dysfunction and death through tunneling nanotubes. Neuron, 112(18), 3106-3125.

[5] Rocca, C. J., Goodman, S. M., Dulin, J. N., Haquang, J. H., Gertsman, I., Blondelle, J., … & Cherqui, S. (2017). Transplantation of wild-type mouse hematopoietic stem and progenitor cells ameliorates deficits in a mouse model of Friedreich’s ataxia. Science translational medicine, 9(413), eaaj2347.

Date Posted: September 21, 2026

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Intermittent Fasting Shows Promise in a Huntington’s Trial

In a pilot study, patients engaging in intermittent fasting demonstrated improvements in Huntington’s disease, a neurodegenerative condition currently considered untreatable. However, the study’s size and limitations call for more research [1].

Fast to survive

Huntington’s disease is an inherited, progressive neurodegenerative disorder caused by an expansion of a repeated DNA sequence in the HTT gene, which encodes the huntingtin protein. Like many neurodegenerative diseases, it is also age-related, with average age of onset between 30 and 50 (juvenile onset happens in about 5% to 10% of cases). The disease affects movement, cognition, and behavior. Although the mutation is the underlying cause, environmental factors may influence when symptoms emerge and how the disease progresses [2].

Currently, no disease-modifying treatments for Huntington’s exist. However, studies in mouse models have shown benefits from intermittent fasting (also known as time-restricted eating, TRE). This led the authors of the new study from Oregon Health & Science University, published in Nature Metabolism, to set up a small pilot trial of TRF in Huntington’s patients.

Twenty people with early-stage Huntington’s completed the study. Their average age was 45, and half were women. The researchers excluded people with unstable weight, high malnutrition risk, significant medical conditions, or cognitive impairment severe enough to prevent participation. Importantly, 60% started with an overweight or obese BMI.

Huntington’s score improves

After a one-week period recording their usual habits, participants adopted a self-selected eating window of 6 to 8 hours for 12 weeks. All participants chose relatively late schedules, with eating beginning between 10 a.m. and 1 p.m. and ending between 6 p.m. and 8 p.m.

Importantly, people with Huntington’s can experience unintended weight loss, which a shorter eating window might exacerbate. However, most patients were able to both adhere to the protocol and largely maintain their weight (a non-significant average loss of 1.12 kilograms was recorded), alleviating the researchers’ concerns.

Having established feasibility and tolerability, the researchers compared neurological assessments at baseline and on follow-up. The composite Unified Huntington’s Disease Rating Scale, a metric combining motor symptoms, functional capacity, and cognitive performance, improved by an average of 0.50 points. This study did not include a control group, but the authors note that this score typically declines by approximately one point per year in early-stage disease. While there was a clear improvement in two of the cognitive tests, the motor score improved modestly, and its significance did not survive multiple-testing correction in the primary analysis.

“This is the first time this approach has been formally studied in people with Huntington’s disease,” said Russell Wells, a fourth-year OHSU medical student and lead author of the study. “We found that participants were able to follow the eating schedule, maintain their weight and show encouraging improvements in clinical and biological measures that are important in Huntington’s disease. These results suggest time-restricted eating deserves further study in a larger clinical trial.”

Energy metabolism affected

Looking beyond clinical tests, the researchers measured plasma neurofilament light (NfL), a structural nerve-fiber protein that can enter the blood when nerves are injured. NfL decreased over the intervention period: the mean individual percentage reduction was 12.6%, while the median reduction was 6.4%. Although a decrease in NfL does not prove slowing of neurodegeneration, earlier longitudinal research specifically reports rising NfL levels as Huntington’s progresses.

“We saw a reversal of the trend we would normally expect,” Wells said. “Neurofilament light typically rises as neurodegeneration continues, but after three months we observed a significant decrease. For a pilot study, that was a remarkable finding.”

The clinical and NfL findings raised a mechanistic question: did the intervention alter cellular energy metabolism, which is disrupted in Huntington’s? The researchers isolated peripheral blood mononuclear cells, a group of circulating immune cells that includes lymphocytes and monocytes, and measured oxygen consumption.

After the intervention, the cells showed higher respiration. The team also found that this increased respiration was linked to increased production of the cellular energy currency ATP. Nonmitochondrial oxygen consumption increased as well.

“One theory is that fasting acts as a mild stressor that prompts cells to become more efficient,” Wells said. “If cells, including brain cells, become better at producing energy and handling stress, they may be more resilient to the disease process.”

The study had several important caveats, apart from lacking a control group and blinding. For instance, the participants also received nutritional guidance and physical-activity recommendations. The average amount of self-reported physical activity rose by 37 minutes a week, while calorie consumption dropped slightly. At least some of the improvement could have originated from these factors rather than from TRE itself.

“One of the unique aspects of Huntington’s disease is that some people know years in advance that they carry the genetic mutation,” Wells said. “That creates a window of opportunity to explore interventions that might delay onset or slow progression. Lifestyle approaches such as time-restricted eating could someday become an important part of that strategy.”

Yes I will donate❤️

Literature

[1] Wells, R.G., Neilson, L.E., McHill, A.W. et al. (2026). Effects of time-restricted eating in early-stage Huntington’s disease: a pilot study. Nat Metab.

[2] Novati, A., Nguyen, H. P., & Schulze-Hentrich, J. M. (2022). Environmental stimulation in Huntington disease patients and animal models. Neurobiology of Disease, 171, 105725.

[3] Wang, H. B., et al. (2018). Time-restricted feeding improves circadian dysfunction as well as motor symptoms in the Q175 mouse model of Huntington’s disease. eNeuro, 5(1), ENEURO.0431-17.2017.

Date Posted: September 18, 2026

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Thymus Grafts Grow in Mouse Spleens, Restoring Immunity

In a new study, thymic tissue implanted in the spleen improved immune responses against viruses and tumors and reversed age-related thymic involution in mice [1].

Growing one organ inside another

The thymus is a small but crucial organ, where T cells mature to become the backbone of our adaptive immune system. There, they acquire their ability to recognize diverse threats along with mechanisms that stop them from attacking the body’s own cells (self-tolerance).

Unfortunately, as we age, the thymus undergoes involution, the progressive loss and disorganization of functional tissue [2]. Chemotherapy, radiation, infections, and other stresses can also damage it. Some children are born without functional thymi, and some patients have their thymi removed.

Existing approaches try to stimulate the remaining thymus tissue or reconstruct the organ using cellular therapies and engineered tissues. However, the task becomes especially difficult when the organ is absent or severely damaged.

Transplantation offers another way: donor thymic tissue can become a new site of T-cell development elsewhere in the body. Cultured thymus tissue implanted into thigh muscle is already used to restore immunity in children with congenital thymic deficiency, but recovery is slow and often incomplete [3].

In a new study published in Advanced Science, a group of Chinese scientists suggests a novel approach: growing thymic tissue in the spleen. This organ has a rich blood supply and hosts a lot of immune cells. Other splenic cells secrete useful growth signals and extracellular matrix. The organ can even support the production of blood cells under certain conditions and is especially immune-tolerant, which makes it the perfect destination for allogeneic (foreign) transplants.

Almost like a normal thymus

The researchers began with neonatal thymus tissue from C57BL/6J mice. Recipients were young BALB/c nude mice, which lack normal thymic development and have profound T-cell deficiency.

Thymus transplantation caused severe adverse reactions by the host’s body (graft-versus-host disease). Thymic tissues contain many developing T cells, so the authors first needed to remove these potential attackers while preserving the tissue itself.

Having established the transplantation protocol, the researchers implanted cultured thymic fragments into either the spleen or quadriceps muscle. Thymic fragments grew faster and formed organized tissue earlier in the spleen. By two weeks, splenic grafts already contained distinct cortical and medullary regions – the two major thymic compartments that support different stages of T-cell development. Muscle grafts were smaller, less organized, and partly necrotic.

Both graft types grew, but splenic grafts reached approximately half the normal thymus weight, much more than muscle grafts. The latter eventually developed a recognizable cortical and medullary organization but remained smaller.

The spleen expressed more thymic development factors and contained more relevant precursor cells than muscle. It also expressed more hemoglobin, consistent with its rich blood supply. However, the study does not show how much each of these factors contributed to the spleen’s superiority compared to muscle.

Circulating T cells appeared after splenic transplantation, and their numbers increased until approximately week eight. However, total T-cell counts remained substantially below normal controls. Recovery was stronger for CD8⁺ cells than for CD4⁺ cells, whose counts stabilized at approximately half the control level.

T cells from recipients of splenic drafts proliferated at levels comparable to controls. When challenged with ovalbumin, an antigen often used in such experiments, treated mice developed antigen-responsive cells, unlike untreated nude mice. Importantly, the response was triggered by the host’s own antigen-presenting cells. Regenerated CD4⁺ T cells also showed a broad receptor repertoire: they were successfully “educated” to counter a wide range of pathogens.

Splenic graft recipients developed less graft-versus-host disease than muscle-graft recipients. Histology, measurements of liver functions, and several inflammatory markers did not reveal major injury. Having established the method in animals lacking a functional thymus, the authors moved to naturally aged mice, transplanting neonatal thymus fragments into 20-month-old animals of the same genetic background. Splenic grafts grew and formed organized thymic tissue in aged recipients. They were larger and had more developing T cells than muscle grafts. Naïve T-cell counts improved relative to controls.

Effective response to infections and cancer

The authors returned to the original nude-mouse model to see whether T-cell restoration translated into protection from infections. Following vesicular stomatitis virus infection, graft recipients had activated T cells and controlled infection much better than untreated nude mice. At ten days, splenic-graft recipients had less detectable viral material and less injury, broadly resembling immunocompetent controls.

The researchers then challenged the mice with tumor cells. Splenic graft recipients demonstrated restricted growth of B16 melanoma compared with untreated nude mice. Their tumors were smaller and contained more infiltrating T cells, with outcomes broadly resembling those of normal controls.

The researchers also implanted human HCT116 colorectal cancer cells. Tumors formed in all untreated nude mice but in none of the splenic-graft recipients, whose level of rejection resembled that of immunocompetent mice.

Finally, the researchers asked whether the effect extended to human tissue. They used immunodeficient mice that had received cryopreserved human thymic fragments and human blood-forming stem cells from the same donor. Groups received no transplant, thymus alone, stem cells alone, or stem cells combined with thymus implanted into spleen or muscle.

Human thymic tissue survived and retained organized architecture in the spleen more effectively than in the muscle. Muscle grafts frequently had necrotic regions, and some became undetectable. Thymus-only recipients produced few circulating human T cells, while adding human stem cells resulted in much stronger T-cell reconstitution.

Yes I will donate❤️

Literature

[1] Wang, S., Zhang, Z., Dai, F., Yin, Z., Xing, Z., Li, Y., … & Dong, L. (2026). Intrasplenic Thymus Organogenesis from Injectable Tissue Fragments Restores Functional T‐Cell Immunity. Advanced Science, e77358.

[2] Liang, Z., Dong, X., Zhang, Z., Zhang, Q., & Zhao, Y. (2022). Age‐related thymic involution: Mechanisms and functional impact. Aging cell, 21(8), e13671.

[3] Markert, M. L., Boeck, A., Hale, L. P., Kloster, A. L., McLaughlin, T. M., Batchvarova, M. N., … & Mahaffey, S. M. (1999). Transplantation of thymus tissue in complete DiGeorge syndrome. New England Journal of Medicine, 341(16), 1180-1189.

Date Posted: September 17, 2026

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Clearing Damaged Mitochondria to Fight Skin Photoaging

Researchers publishing in Aging Cell have found that a cocktail of molecules released by human umbilical cord mesenchymal stem cells (hUC-MSCs) can mitigate sun-induced skin aging (photoaging) in mice by restoring their cells’ ability to get rid of their own damaged mitochondria (mitophagy).

Wrinkles are only a small part of the problem

Chronic exposure to ultraviolet light is the main driver of photoaging, which is characterized by the accumulation of senescent cells in the skin along with the depletion of DNA-protecting lamins [1]. It causes skin to become thickened, wrinkled, and rough while accumulating visible veins [2]. This damage is more than cosmetic; photoaging can lead to precancerous lesions along with cancer itself [3]. Retinoids and other antioxidants have been found to have some effects but cannot completely reverse this damage [4], and laser-based treatments may be expensive and painful while causing other symptoms [5].

This work focuses on the relationship between the accumulation of damaged mitochondria (mitochondrial dysfunction) and age-related inflammation in the absence of pathogens (inflammaging). Mitochondrial dysfunction leads to the activation of the inflammatory cGAS-STING pathway [6], which increases the production of cytokines such as IL-6 and IL-8 and is known to drive inflammaging in other tissues [7].

The compounds secreted by hUC-MSCs, including proteins and exosomes, are collectively referred to as the secretome, which has been found to treat diabetic skin lesions in a mouse model [8]. Previous work had involved some of these components, and we have reported extensively on the use of exosomes. However, this team utilized the secretome as a whole, attempting to determine the extent of its effects against mitochondrial dysfunction and inflammaging in the context of skin photoaging.

Broad and significant effects

The researchers initially ran a mouse experiment in which they shaved patches of skin and exposed the animals to 40 days of UVA and UVB light calibrated to mimic chronic sun exposure, then treated some of the irradiated skin with a topical hUC-MSC-derived secretome. Compared to the control group, the treated mice showed less epidermal thickening, better hydration, improved elasticity, and less water loss through the skin barrier. Skin collagen, which typically fragments and depletes with ultraviolet exposure, was largely preserved as well. Two markers of cellular senescence, p16 and p21, were also reduced in these animals.

The team also irradiated human skin cells (HaCaT keratinocytes) with UVB and cultured some of them in the presence of an MSC-derived secretome. The results were similar to those seen in mice: compared to the control group, the treated cells were less likely to become senescent as measured by the well-known biomarker SA-β-gal, and they had less UV-induced reduction of Lamin B1.

As expected, compared to mice that were never exposed to ultraviolet radiation at all, exposed mice had more dysfunctional mitochondria and a significant reduction in mitophagy; this was evidenced by increases in mitochondrial proteins, a decrease in the mitophagy biomarker LC3B-II, and similar decreases in the related factors PINK1 and Parkin. These researchers found that treatment with the MSC secretome mitigated this dysfunction completely, as markers of functional mitophagy were indistinguishable from those of the UV-unexposed control group, and these findings were also replicated in vitro with HaCaT cells. Similarly, treatment with this secretome reduced activation of cGAS/STING and diminished the production of downstream inflammatory cytokines, both in mouse skin and in cultured cells.

A clear causal chain

Mitophagy was confirmed to be the key driver of the hUC-MSC secretome’s effects. Alongside administration of Mdivi-1, which blocks mitophagy, this secretome was found to be ineffective. Directly blocking STING through the H151 inhibitor, or forcing mitophagy through the compound CCCP, had similar effects as secretome administration in vitro. A series of in vivo experiments utilizing combinations of these compounds confirmed this hierarchical relationship: the hUC-MSC secretome induces mitophagy, which fights cGAS/STING-related inflammation, which is responsible for many of the downstream negative effects of photoaging.

Of course, these experiments were conducted with mice and a single immortalized human skin cell line; as human skin is thicker than mouse skin and has likely suffered different long-term damage over a longer lifespan, the results of a clinical trial may be different. These researchers also chose to use the MSC secretome as a whole rather than specific proteins or exosomes, which obfuscates the contributions of its various components.

However, this study confirms that the skin, just like the heart and brain, experiences inflammaging driven by mitochondrial dysfunction. If the particular factors involved in the hUC-MSC secretome’s effects against this dysfunction can be identified, clinically tested, and produced, such a product may be more effective than current treatment methods.

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Literature

[1] Zhang, H., Xiao, X., Wang, L., Shi, X., Fu, N., Wang, S., & Zhao, R. C. (2024). Human adipose and umbilical cord mesenchymal stem cell-derived extracellular vesicles mitigate photoaging via TIMP1/Notch1. Signal transduction and targeted therapy, 9(1), 294.

[2] Dorf, N., & Maciejczyk, M. (2024). Skin senescence—from basic research to clinical practice. Frontiers in medicine, 11, 1484345.

[3] Sun, Z., Zheng, Y., Wang, T., Zhang, J., Li, J., Wu, Z., … & Tan, Y. (2025). Aloe vera gel and rind-derived nanoparticles mitigate skin photoaging via activation of Nrf2/ARE pathway. International journal of nanomedicine, 4051-4067.

[4] Zhang, H., Xiao, X., Wang, L., Shi, X., Fu, N., Wang, S., & Zhao, R. C. (2024). Zhang, J., Li, Z., Song, X., Cai, P., & Liu, Q. (2025). Ginsenoside CK and retinol on UVA-induced photoaging exert the synergistic effect through antioxidant and antiapoptotic mechanisms. Scientific Reports, 15(1), 16664.

[5] Zhu, J., Chang, R., Han, Y., Xi, Q., Jiang, S., Shang, Y., … & Lin, X. (2025). Comparison of Intense Pulsed Light With Nonablative Fractional Laser and Picosecond Alexandrite Laser With Diffractive Lens Array for Noninvasive Facial Rejuvenation. Lasers in Surgery and Medicine, 57(2), 195-203.

[6] Meng, S., Duan, J., Zhao, J., Zhou, Z., Sun, B., Xu, Y., … & Wang, H. (2026). Impairment of mitochondrial quality control exacerbates diabetes-related atrial fibrillation by cGAS-STING signaling pathway and cardiomyocyte-macrophage crosstalk. Theranostics, 16(4), 1701.

[7] Li, H., Cai, R., Zhou, Y., Jiang, Y., & Tan, S. (2025). cGAS-STING signaling in brain aging and neurodegeneration: molecular links and therapeutic perspectives. Journal of neuroinflammation, 22(1), 235.

[8] Chen, W. H., Lai, W. Y., Le, D. C., Hsing, J. C., Ngo, M. H. T., Kao, C. X., … & Huang, Y. H. (2025). Secretome from human placenta-derived mesenchymal stem cells repairs mechanically induced meniscus injury in mice by activating the proliferation and suppressing the apoptosis of endogenous meniscus progenitor cells. Stem Cell Research & Therapy, 16(1), 565.

Date Posted: September 15, 2026

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An Entirely New Target for Fighting Senescence

Researchers have established how a protein that is nearly absent in the literature, PTCHD4, is linked to cellular senescence.

Very little previous work

In most papers, after a customary discussion of the mechanics of cellular senescence and current methods of handling it and its repercussions, the researchers go on to discuss previous work relating to the particular approach at hand. However, that does not pertain to this paper; PTCHD4 is only known as being structurally related to PTCH1, which affects the Hedgehog signaling pathway [1]. While some work has linked dysregulation of Hedgehog pathways to accelerated neurodegeneration [2], the specific role of PTCHD4 was not clear.

The researchers found that, when exposed to the genotoxin bleomycin, PTCHD4 increases alongside inflammation markers in a variety of cells, including human fetal lung diploid fibroblasts, mouse embryonic fibroblasts (MEFs), alveolar epithelial type II cells (AEC2s), human umbilical vein endothelial cells (HUVECs) and adult retinal pigment epithelial cells. Aging Atlas data confirmed this upregulation in other types of cells as well, and NCBI data listed this molecule as being disease-associated: its presence is negligible under ordinary conditions.

The team then examined young mice, old mice, and progeric mice, staining for PTCHD4 alongside the senescence biomarker p16. The two biomarkers were expressed in similar quantities among each group in multiple tissues. Similar results were found in human tissue samples; idiopathic pulmonary fibrosis (IPF) patients expressed more PTCHD4 in their lungs than people without the disease, and human lung cells expressing PTCHD4 were more likely to also express established senescence markers.

Significant effects on senescence

The next experiment involved creating MEFs that do not express PTCHD4 and then driving them senescent through replication. PTCHD4 was found to be a critical driver of senescence in this group; after an average of eight passages, ordinary MEFs exhibited signs of senescence, such as the key biomarker SA-β-gal, while this did not occur to the PTCHD4-deficient MEFs until an average of passage 14.

This line of experimentation continued with PTCHD4-overexpressing MEFs, which began exhibiting senescence-related features such as SA-β-gal early in passage 5. Similar results were found in AEC2s; the inflammatory biomarkers IL6 and IL8, along with SA-β-gal, were upregulated alongside PTCHD4 overexpression.

This testing continued with live mice. The researchers utilized mice that do not express PTCHD4 along with wild-type mice, and they exposed both groups to D-galactose, which mimics many of the symptoms of natural aging. The mice that did not express PTCHD4 were much more resistant to D-galactose than wild-type mice, and there were no detectable physical or biochemical problems caused by this absence.

The team then continued with naturally aging animals. They found that mice that do not express PTCHD4 naturally live months longer than wild-type mice, and mice without it apparenly do not develop white hair the way that wild-type animals do.

A further experiment involved subjecting mice to bleomycin, which harms lung function in a way that mimics IPF in people. As expected, the mice exhibited features of lung fibrosis within 21 days. However, the PTCHD4-less mice suffered from fewer symptoms of the disease, retaining more lung capacity, less immune infiltration, less destruction of alveolar tissues, and less fibrosis than wild-type mice.

A well-known signaling pathway

In this study, PTCHD4 was found to have no effects on the Hedgehog pathway or related genes. Instead, its effects were found to be due to AKT signaling. AKT activation normally increases with aging, but a lack of PTCHD4 diminished this. The team created MEFs that do not express PTCHD4 but express AKT through a different construct, and these MEFs were not protected by their lack of PTCHD4. Similar experiments involving the direct expression of AKT in other cell types confirmed these results, recapitulating the effects of PTCHD4.

The researchers believe that “PTCHD4 may represent a candidate target for senescence-associated interventions” and that there is “a potential role for PTCHD4 in age-related fibrotic disease.” However, this is an initial study. Further work will need to be done to confirm these results, elucidate the relationship of PTCHD4 and AKT, ascertain any side effects of eliminating or suppressing PTCHD4, and determine if PTCHD4 can be targeted by interventions.

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Literature

[1] Harvey, M. C., Fleet, A., Okolowsky, N., & Hamel, P. A. (2014). Distinct effects of the mesenchymal dysplasia gene variant of murine Patched-1 protein on canonical and non-canonical Hedgehog signaling pathways. Journal of Biological Chemistry, 289(15), 10939-10949.

[2] Esmaeli, M., Dehabadi, M. D., Ghanbari, A., & Yancheshmeh, F. S. A. (2025). The role of Sonic Hedgehog (SHH) in the formation of motor neurons and neurodegenerative diseases. Discover Medicine, 2(1), 231.

Date Posted: September 14, 2026

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Mitochondrial Performance May Strongly Influence Learning

A team of researchers has discovered that mitochondrial health and location may be critical to why cognitive plasticity decreases with age.

Old mammals and new tricks

The adage ‘you can’t teach an old dog new tricks’ is true across a wide variety of organisms; neural plasticity decreases with age in rodents, non-human primates, and people [1]. This form of cognitive decline stems from changes in individual cells: the dendrites of prefrontal cortex neurons become less plastic [2], and the biochemistry of the synapses is altered [3]. This is accompanied by changes in brain metabolism [4].

This lack of cognitive plasticity often manifests itself in cognitive inflexibility and perseveration: needless, constant repetition when the reason for the original behavior has long since passed. To diagnose this in rodents, researchers often use an attention set shifting task that tests the animals’ ability to learn and apply novel facts when circumstances change [5].

The precise relationship between the brain’s physical changes with aging and the resulting lack of behavioral plasticity, especially at the individual level, has not been fully elucidated. These researchers, therefore, conducted both behavioral and in-depth proteomic testing to learn more about this relationship.

Changing the rules halfway through

In this study, the researchers had Black 6 mice learn two different sets of rules. In the first part, the mice would learn that pressing a button with two vertical lines or two horizontal lines would yield a food reward. In the second part, however, the rule changed; the lines stopped mattering, and it only mattered whether the button was the one on the left or the right.

Two different strains of Black 6 mice performed much differently on this task with aging. Overall, C57BL/6N mice demonstrated a significant age-related decline in their ability to learn the new rule. On the other hand, C57BL/6J mice, as a whole, showed much less of a decline; only some of the older mice of this strain performed notably worse than their younger counterparts. The researchers, therefore, chose to conduct all their future experiments on the J strain, looking for the reasons why some mice performed worse than others.

Many age-related changes in neuron structure appeared to have no discernible relationship to this decline. A loss of smaller dendrites, which lack spines, was not found to be correlated to this task, nor was a large axon-spine interface. The researchers also examined astrocytes around the synapses, but those were neither correlated with aging nor had any impact on this task.

Instead, presynaptic mitochondria found in larger axon-spine interfaces, despite not being associated with aging overall, were related to this form of cognitive decline in aged mice. The researchers then looked more closely at the involved proteins and genes, finding many candidates that appeared to be related, although the number of mice was too small to draw completely firm conclusions. The researchers’ most interesting finding was that differentially expressed genes with aging were largely different from those related to cognitive decline in these mice; therefore, this team concluded that the “neural mechanisms determining individual variability in cognitive inflexibility are distinct from chronological aging processes.”

As expected, many of the genes associated with cognitive decline involved the mitochondria, specifically the regulation of mitochondrial metabolism. Some of the genes were directly related to synapse management itself. Better mTOR signaling and, unsurprisingly, better amyloid protein handling were found to be associated with better cognitive performance. Mitochondrial proteins found in synapses were specifically found to be “more abundant in aged mice with greater cognitive inflexibility.”

Reducing oxidative stress appears to help

The researchers then performed another experiment using the mitochondrial antioxidant MitoQ, which had previously performed well against memory loss in mouse models of Alzheimer’s [6]. While it did not significantly improve the mice’s visual learning ability, it was found to have beneficial effects on the attention set task after 20 weeks of administration; the treated aged mice were able to adapt to the new rule faster than the untreated mice. It diminished some of the mitochondrial proteins in synapses, specifically those related to apoptosis, and it upregulated proteins related to aerobic respiration.

This is exploratory research, and, other than mitochondrial health and oxidative stress as a whole, the paper offers suggestions but not biochemical intervention targets. It suggests that presynaptic mitochondria may need to be specifically targeted, and it highlights the possibility that reactive oxygen species produced by mitochondria may be having deleterious downstream effects on neurons’ structural plasticity. Further work will need to be done to determine if there is any novel mitochondrial target that may restore older people’s ability to learn new things.

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Literature

[1] Burke, S. N., & Barnes, C. A. (2006). Neural plasticity in the ageing brain. Nature reviews neuroscience, 7(1), 30-40.

[2] Bloss, E. B., Janssen, W. G., Ohm, D. T., Yuk, F. J., Wadsworth, S., Saardi, K. M., … & Morrison, J. H. (2011). Evidence for reduced experience-dependent dendritic spine plasticity in the aging prefrontal cortex. The Journal of Neuroscience, 31(21), 7831-7839.

[3] Morrison, J. H., & Baxter, M. G. (2012). The ageing cortical synapse: hallmarks and implications for cognitive decline. Nature reviews neuroscience, 13(4), 240-250.

[4] Lee, J., & Kim, H. J. (2022). Normal aging induces changes in the brain and neurodegeneration progress: review of the structural, biochemical, metabolic, cellular, and molecular changes. Frontiers in aging neuroscience, 14, 931536.

[5] Heisler, J. M., Morales, J., Donegan, J. J., Jett, J. D., Redus, L., & O’connor, J. C. (2015). The attentional set shifting task: a measure of cognitive flexibility in mice. JoVE (Journal of Visualized Experiments), (96), e51944.

[6] McManus, M. J., Murphy, M. P., & Franklin, J. L. (2011). The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease. The Journal of Neuroscience, 31(44), 15703-15715.

Date Posted: September 11, 2026

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Lung Fibrosis Drug Lowers Biological Age Estimates

Six different aging clocks detected younger blood protein profiles in patients taking the experimental lung-fibrosis drug rentosertib. This suggests possible anti-aging effects, but separating those from the narrower benefits of treating fibrosis remains a challenge [1].

The AI-developed drug

Many drugs developed for particular diseases act on aging-related biological processes. That creates an opportunity: a clinical trial could investigate both whether a drug treats its intended disease and whether it has broader effects on aging. Ordinary clinical measurements cannot establish those broader effects, but we now have biological age clocks that closely track chronological age or predict mortality risk [2]. These clocks have been used in numerous trials as proxies to estimate the intervention’s effect on aging.

In a new study published in Nature Biotechnology, the researchers analyzed blood samples from a Phase 2a trial whose results were published last year [3]. That 12-week, randomized, double-blind, placebo-controlled trial tested rentosertib, an inhibitor of the kinase TNIK, which has been implicated in several aging-related processes [4].

Rentosertib was developed by the longevity biotech company Insilico, using a proprietary AI-based drug discovery platform, to treat idiopathic pulmonary fibrosis (IPF), a progressive disease in which excessive scar tissue compromises lung function. IPF is age-related, with a mean age of onset around 65 years, and aging processes such as cellular senescence and inflammation are heavily involved.

The new analysis included 42 of the trial’s 71 participants. Alongside placebo, the trial tested three regimens: 30 milligrams once daily, 30 milligrams twice daily, and 60 milligrams once daily.

Lower biological age readings

The researchers used six different proteomic clocks, which analyze protein levels in blood. The proteomic clocks’ appeal is partly interpretability: researchers can identify which proteins affect the readings and connect them to known biological processes more directly than is often possible with methylation-based clocks. The clocks were developed by different teams, using data from UK Biobank, including one clock developed by Insilico itself. Four of the clocks were trained on chronological age, and two on mortality.

All six clocks detected lower predicted biological ages in patients taking rentosertib, although not at every dose or visit. After four weeks, the four chronological age-based clocks rated patients taking 60 milligrams once daily (the single-dose regimen) roughly three years younger, on average, than at the start of treatment. These changes were statistically significant compared with placebo. However, the two clocks trained to predict mortality risk did not show a significant change at that dose at week four.

Patients taking 30 milligrams twice daily (the split-dose regimen) showed the most consistent decreases across both types of clocks. The largest reductions in predicted biological age appeared by week four, with little additional change over the remaining eight weeks.

These results essentially mean that patients’ blood protein profiles became more similar to those associated with younger people. They do not, however, establish that the treated patients regained years of youth or would live longer.

Is there a broad anti-aging effect?

Looking beyond the clock readings, the researchers found that treatment changed the levels of 326 blood proteins, including proteins involved in fibrosis, metabolism, and cellular stress responses. Most changes in the two higher-dose groups persisted throughout the trial or appeared later in treatment, suggesting that the drug continued affecting patients’ biology even after predicted ages plateaued.

The researchers then examined which proteins contributed most to the younger age estimates. A fibrosis-associated protein, LTBP2, stood out as a major contributor. It was used by all six clocks, which raises the question of whether their agreement mainly reflects the drug’s effect on fibrosis, rather than broader slowing of aging.

To explore whether the lower age estimates reflected more than improvement in fibrosis, the researchers compared changes in predicted age with changes in lung function. The two did not closely track each other. This suggests that improved lung function alone might not explain the clock changes, although lung function does not capture every aspect of IPF.

The team then compared the treatment-induced protein changes with differences between younger and older participants in UK Biobank. With the split dose, proteins associated with aging tended to move in the opposite direction: those found at higher levels in older people tended to decrease, and vice versa. This pattern was not statistically significant with the single daily dose.

Finally, the researchers examined proteins associated with cellular senescence. These proteins tended to increase in the placebo group but decrease with treatment, suggesting that rentosertib might reduce senescence-associated activity, although the researchers did not directly measure senescent cells in tissues.

These findings strengthen the case for investigating rentosertib as a potential geroprotector. However, because fibrosis, metabolism, and senescence are closely connected, they still cannot definitively establish whether the drug affects aging beyond its benefits for IPF.

“This study illustrates how biomarkers of aging can be incorporated into conventional clinical trials,” Vadim Gladyshev, a professor of medicine at Harvard Medical School and a coauthor of the study, told Lifespan News. “If validated more broadly, such approaches could allow us to learn not only whether a treatment affects a particular disease, but also whether it influences some aspects of aging biology.”

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Literature

[1] Zhavoronkov, A., Galkin, F., Chen, S., Ren, F., Aliper, A., Durymanov, M., … & Gladyshev, V. N. (2026). Integration of proteomic aging clocks in a phase 2a clinical trial supports simultaneous geroprotective assessment. Nature Biotechnology, 1-13.

[2] Argentieri, M. A., Xiao, S., Bennett, D., Winchester, L., Nevado-Holgado, A. J., Ghose, U., … & van Duijn, C. M. (2024). Proteomic aging clock predicts mortality and risk of common age-related diseases in diverse populations. Nature medicine, 30(9), 2450-2460.

[3] Xu, Z., Ren, F., Wang, P., Cao, J., Tan, C., Ma, D., … & Zhavoronkov, A. (2025). A generative AI-discovered TNIK inhibitor for idiopathic pulmonary fibrosis: a randomized phase 2a trial. Nature medicine, 31(8), 2602-2610.

[4] Ewald, C. Y., Pulous, F. E., Lok, S. W. Y., Pun, F. W., Aliper, A., Ren, F., & Zhavoronkov, A. (2024). TNIK’s emerging role in cancer, metabolism, and age-related diseases. Trends in pharmacological sciences, 45(6), 478-489.

Date Posted: September 11, 2026

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Your Personal Longevity Assistant: Evipedia Grok Bot

With Grok Bot, SpaceXAi has created something really special and helpful. And the Evipedia Grok Bot turns this gem into something even more precious. A specialized AI assistant offering an evidence-based 2nd opinion on health and longevity interventions. It integrates Grok, the AI4L persona, the Evipedia MCP server, and Evipedia-hosted search into one super-useful companion.

What Evipedia Grok Bot will do for you

The bot will allow you to have interactive conversations about a wide range of health and longevity interventions. It delivers helpful 2nd opinions on these topics, and all its answers are grounded in the same principles and behavior used by Evipedia and AI4L:

Tailored for the Longevity Community — answers are framed for risk-aware adults actively optimizing their health, not for the general population
Evidence First — conclusions rest on human clinical trials and meta-analyses; conflicting, thin, or absent evidence is named as such rather than smoothed over
Graded Findings — each benefit and risk carries an explicit High, Medium, Low, or Speculative grade and, where the literature supports one, a magnitude
The Full Picture — interventions are looked at across mechanism, benefits, risks, interactions, protocol, monitoring, and open research
Commercial Interests — when the evidence comes from parties with a financial stake in the intervention, or from an organization whose members profit from the position it endorses, conflicts are named on every side of the debate
Evipedia Lookup — health and longevity questions are checked against the evidence reviews on evipedia.ai before the model answers from memory
Plain Language — acronyms and jargon get a short explanation at first use, and scientific nomenclature follows field convention
Verified Links — every PMID, NCT ID, and DOI is retrieved and checked before it is shown; a URL that cannot be verified is omitted rather than guessed
Review Suggestions — when an intervention under sustained discussion has no Evipedia review, the model offers to suggest it to the Evipedia editorial team or points to generating an evidence review using the AI4L prompt

What’s in Evipedia

Evipedia is a comprehensive, continuously updated online encyclopedia that provides much-needed, accurate, and up-to-date information on a wide range of health and longevity-related interventions.

Free to Use — Evipedia is completely free to use and open to everyone. We built Evipedia as a backbone tool for the whole longevity and rejuvenation community. Our goal is to empower individuals with knowledge to make informed decisions about their health and longevity.
770+ Evidence Reviews — Including whole-body therapies, brain health, skin rejuvenation, hormone optimization, peptides, psychedelics, medications, blood and plasma therapies, complementary cancer approaches, foundational habits, diets, foods, probiotics, botanicals, isolates, and many more.
A Dual Structure for Every Entry — Each intervention has a one-page Quick Reference Sheet for an at-a-glance protocol, benefits, risks, contraindications, and monitoring, plus a Full Evidence Review for in-depth analysis.
Continuous Updates — Entries are continuously updated to reflect the latest developments in health and longevity. On average, reviews are refreshed every 4-6 weeks, ensuring access to the most current information available.
Full Audit and Quality Transparency — Every “Quick Reference Sheet” and “Evidence Review” on Evipedia includes an Audit Report that outlines the detailed audit criteria and the history of audits and fixes applied to the documents.
Stable Permalinks – Beautiful Sharing Cards — Every intervention has a fixed, short URL and a purpose-designed social sharing card — ideal for citing a compound in a supplement stack or anchoring a claim in an online discussion.
AI & Agent-friendly, Extensive Integration Support — Built as a backbone service for the longevity and rejuvenation community, Evipedia features a wide variety of AI integration tools and an easily accessible API. All are free to use, under an AI- and agent-friendly site policy and the Creative Commons 4.0 license.
Built on AI4L — Evipedia is built on top of our open-source AI4L framework, which enables anyone to create high-quality, evidence-based reviews of health and longevity interventions. At the core of AI4L is our novel “Audit-Driven Prompting” approach to generate hallucination-free, accurate, and well-structured reviews using frontier AI models.

About Forever Healthy

Forever Healthy Foundation is a private, humanitarian initiative with the mission of enabling people to vastly extend their healthy lifespan. More at forever-healthy.org

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Date Posted: September 10, 2026

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From World Cup Champions to Longevity Champions

Fresh from Spain’s spectacular victory in the 2026 FIFA World Cup, Madrid is preparing for another kind of world-class gathering: one focused not on winning more years of sporting glory, but on winning more healthy years of life.

On September 30 and October 1, 2026, the International Longevity Summit Madrid 2026 will bring together leading scientists, physicians, entrepreneurs, investors and futurists to explore one of humanity’s greatest challenges—and potentially greatest opportunities: extending healthy human life.

Organized by the International Longevity Alliance, the Summit comes to a city uniquely positioned to lead the global conversation on longevity. Spain has the highest life expectancy in the European Union, while the Comunidad de Madrid has recorded the highest life expectancy of any EU region, reaching the remarkable landmark of 85.7 years according to Eurostat. Madrid may therefore be more than simply a great European capital; it could increasingly be considered a “Blue Zone 2.0”: a modern, dynamic metropolis where exceptional longevity meets cutting-edge science, biotechnology and innovation.

And now, after Spain’s national team, La Roja, captured the 2026 FIFA World Cup, Spain can proudly claim another world-leading achievement. In July, Spain defeated Argentina 1–0 after extra time to win its second men’s World Cup title, adding a new chapter to a country already renowned for its health, lifestyle and longevity.

From world champions on the football field to potential champions of healthy longevity, Spain is demonstrating that the future may belong to those who know how to live—and perhaps someday live much longer.

A new royal home at Spain’s most prestigious medical institution

After the success of previous editions held at the Ilustre Colegio Oficial de Médicos de Madrid (ICOMEM), where the Summit was inaugurated with the participation of the Mayor of Madrid, José Luis Martínez-Almeida, the 2026 edition takes a major institutional step forward.

This year, the Summit will be held at the magnificent Real Academia Nacional de Medicina de España (RANME), the Royal National Academy of Medicine of Spain, the country’s most prestigious medical institution. Founded in 1734, the Academy occupies a unique place in Spanish scientific history. The Academy is under the High Patronage of His Majesty King Felipe VI, underlining the exceptional institutional importance of the venue. The Academy is also historically associated with some of the greatest names in medicine, including Spain’s Nobel laureates Santiago Ramón y Cajal and Severo Ochoa.

Located in the historic heart of Madrid, between the Royal Palace and the Teatro Real, the RANME will provide an extraordinary setting for a conversation that could reshape the future of medicine itself.

From George Church and Ray Kurzweil to Eric Topol and Peter Diamandis

The International Longevity Summit has rapidly become a meeting point for some of the world’s most influential thinkers in longevity, biotechnology, medicine and the future of humanity.

Previous editions of the International Longevity Summit in Madrid have featured an exceptional roster of speakers, including George Church, pioneering geneticist; Ray Kurzweil, futurist and inventor; Steve Horvath, creator of the epigenetic clock; Andrea Maier, longevity physician and researcher; Mehmood Khan, global health and life sciences leader; Liz Parrish, biotechnology entrepreneur; Aubrey de Grey, biomedical gerontologist; Bryan Johnson, entrepreneur and longevity pioneer; María Blasco, molecular biologist and telomere researcher; João Pedro de Magalhães, biogerontologist and aging researcher; and Michael Ringel, biotechnology and pharmaceutical executive—along with many other leading scientists, physicians, entrepreneurs, and innovators from around the world.

The 2026 edition continues and expands this tradition of quality. Among the distinguished participants and speakers announced for 2026 are Eric Topol, cardiologist and digital medicine pioneer; Peter Diamandis, entrepreneur and futurist; Brian Kennedy, aging researcher; Valentin Fuster, cardiologist and cardiovascular scientist; Bashayer Almubarak, longevity and health innovation leader; Guido Kroemer, cell biologist and aging researcher; Steven Austad, biogerontologist; Michel Poulain, demographer and Blue Zones researcher; Michael West, stem cell pioneer; Mike Chan, longevity expert and entrepreneur; Wei-Wu He, biotechnology entrepreneur; Patrick E. Sewell, longevity physician; Ronald Bonilla, dentist and longevity innovator; Tina Woods, health and longevity leader; Daniel Wallerstorfer, geneticist and biotech entrepreneur; David Wood, futurist and longevity advocate; and Kenneth Scott, entrepreneur and longevity advocate—along with many other leading international and Spanish scientists, physicians, entrepreneurs, and innovators.

The program will span the biology of aging, rejuvenation biotechnology, preventive and regenerative medicine, artificial intelligence, health data, biomarkers, the longevity economy and the profound social consequences of potentially dramatic increases in human healthspan.

From conference to scientific marketplace: posters and startup pitches debut in 2026

For the first time, the International Longevity Summit will introduce scientific poster sessions and startup pitches, opening the stage to a new generation of researchers, entrepreneurs and innovators. Through an international Open Call, selected participants will have the opportunity to present research projects, scientific posters, short talks and startup initiatives to an audience of experts, investors, physicians and longevity enthusiasts. The goal is to make the Summit not only a place where established leaders discuss the future, but also a platform where the next generation of breakthroughs, companies and scientific careers can begin.

A distinguished group of prestigious Spanish and international institutions is supporting this historic event, organized by International Longevity Alliance (ILA) at the Royal National Academy of Medicine of Spain (RANME), in collaboration with the Official College of Physicians of Madrid (ICOMEM) and Madrid Innovation. International supporters include European Wellness and Triple Helix Science at the Gold level, as well as Novogenia and Nesa World at the Silver level. The event is also endorsed by leading foundations and organizations, including HealthGevity Nation, Hevolution Foundation, Human Longevity Inc., HumanityPlus, Immortalis, KHL Foundation, Life Extension Foundation, Lifeboat Foundation, Longevity Escape Velocity Foundation, Millennium Project, XPRIZE Foundation, together with innovative companies such as Cenegenics, GERO, and OXANA. This year, the Summit will also welcome a new generation of startups working in healthtech, healthcare innovation and longevity, with the logistical support of CRRATE and StartUp Olé Salamanca.

The 2026 edition aims to further strengthen Madrid’s role as a bridge between Europe, Latin America, North America and the rapidly expanding global longevity economy.

Two days of UNESCO history before exploring the future

The Summit will begin even before the scientific program officially opens. On September 28 and 29, participants will be able to join two special pre-conference excursions to some of the most remarkable UNESCO World Heritage sites surrounding Madrid. The first day will travel south-east to Alcalá de Henares, Aranjuez and Toledo. The second will head north-west to Ávila, Segovia and El Escorial.

The contrast is intentional: participants will explore centuries of Spanish and European history before returning to Madrid to discuss technologies that may transform the future of human life itself. From ancient cathedrals and royal palaces to cellular rejuvenation, artificial intelligence and longevity escape velocity, the International Longevity Summit 2026 promises a journey through both humanity’s past and its possible future.

This summer, Spain has shown the world how to win on the football field. This autumn, Madrid will invite the world to explore how humanity might also win the greatest matches of all: the race against aging!

International Longevity Summit 2026

Dates: September 30 – October 1, 2026

UNESCO World Heritage Tours: September 28–29, 2026

Free registration for the Madrid Longevity March

Venue: Real Academia Nacional de Medicina de España (RANME)

Organizer: International Longevity Alliance

Information and registration: www.LongevitySummit.Madrid

Videos: Teaser · UNESCO Tours · Full 12-minute Promo

Media kit: Images and Clips

General inquiries: info@longevitysummit.madrid

About José Cordeiro

José Cordeiro, PhD, is an engineer from MIT and MBA from INSEAD. He is director of the International Longevity Alliance, vicechair of HumanityPlus, fellow of the World Academy of Art & Science, senior fellow of The Millennium Project, founder of the International Longevity Summit in Madrid, founding faculty of Singularity University in Silicon Valley, former Spanish candidate to the European EurParliament and coauthor of the international bestseller The Death of Death.

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Date Posted: September 10, 2026

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Calcium Mishandling Contributes to Muscle Loss

Researchers have discovered and explained how calcium mishandling in muscle cells leads to long-term muscle weakness in older people.

Calcium is not just for bones

Skeletal muscle cells use calcium ions to control how and when they contract. This activity is modulated by CaMKII, a protein kinase that also regulates muscle adaptations in response to exercise [1] and serves a great many unrelated functions throughout multiple other tissues.

In young tissues, this system works well, with exercise producing reactive oxygen species (ROS) that are used to stimulate muscle growth [1]. However, with aging, this falls apart in multiple ways: calcium ions leak out of where they are supposed to be [2], mitochondria and calcium become uncoupled [3], and, as has been well-known for decades, ROS and oxidative damage are no longer properly mitigated [4]. The authors hypothesized that CaMKII signaling is involved in this dysregulation.

Constant expression weakens muscles

In their first experiment, the researchers examined the muscles of 3.7-month-old mice and compared them to those of 33-month-old mice; 33 months is exceptionally old for a mouse, and mice of that age were provided by the gerontologist Dr. Rafael deCabo. These elderly mice had significantly smaller muscles than the younger group, substantially more CaMKII in muscle tissue, and more evidence of CaMKII activity while at rest. However, the researchers noted that the biomarker they used to detect activity, pT287-CaMKII, is not entirely consistent in various muscle tissues and CaMKII can be modified in many other ways [5].

To determine the effects of constant CAMKII activity in muscle, this team developed a adeno-associated virus (AAV) that caused it to become active only in that tissue. This AAV had local effects, meaning that the researchers were able to inject it onto only one tibialis anterior muscle of each individual mouse; the identical muscle on the other side was injected with a simple fluorescent reporter protein with no significant effects. Interestingly, feedback mechanisms caused natural CAMKII to be suppressed in the muscles that were given this artificial CAMKII increase.

Within less than two months, this increase in constant CaMKII caused the targeted muscles to shrink and become pound-for-pound weaker than the unmodified muscles in the same mice; direct stimulation at multiple frequencies found that the targeted muscles were unable to exert nearly as much force. While it did not impact total mitochondrial number, it had significant negative effects on mitochondrial organization. A similar experiment with a different cohort of mice found that, after nine months, the loss of muscle mass became even more significant.

Some of this muscle loss was found to be driven by inflammation. Blocking the inflammatory signal NF-κB while activating CaMKII blunted some of the effects; the muscles in this group did not become pound-for-pound weaker, but they still lost mass.

Age-related gene expression changes

Gene expression was also significantly impacted. While there were some differences, the impact of constant CaMKII expression was broadly similar to that of natural aging in muscle, and the researchers identified many biochemical pathways that are increased both by natural aging and by increased CaMKII. Most notably, iron-handling pathways were significantly disrupted by CaMKII.

The researchers also injected naturally aged mice with CN19o, which inhibits CaMKII; while individual genes were not significantly affected, the sum total of gene expression was found to move towards a more youthful phenotype. While it did not increase muscle size in 21-month-old mice, suppressing CaMKII in these mice increased their ability to contract.

The researchers hold that age-related constant CaMKII signaling is a significant contributor to sarcopenia. In youth, this signaling is beneficial, but in an aged environment, it is apparently doing more harm than good. However, the researchers did not experimentally validate why constant CaMKII activation has the mitochondrial effects it does, nor did they fully elucidate the connection between calcium and iron signaling. Further work will need to be done to determine if CaMKII is a useful target in people.

Yes I will donate❤️

Literature

[1] Wang, Q., Hernández-Ochoa, E. O., Viswanathan, M. C., Blum, I. D., Do, D. C., Granger, J. M., … & Anderson, M. E. (2021). CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution. Nature communications, 12(1), 3175.

[2] Lamboley, C. R., Wyckelsma, V. L., McKenna, M. J., Murphy, R. M., & Lamb, G. D. (2016). Ca2+ leakage out of the sarcoplasmic reticulum is increased in type I skeletal muscle fibres in aged humans. The Journal of physiology, 594(2), 469-481.

[3] Pietrangelo, L., D’Incecco, A., Ainbinder, A., Michelucci, A., Kern, H., Dirksen, R. T., … & Protasi, F. (2015). Age-dependent uncoupling of mitochondria from Ca2+ release units in skeletal muscle. Oncotarget, 6(34), 35358.

[4] Mecocci, P., Fano, G., Fulle, S., MacGarvey, U., Shinobu, L., Polidori, M. C., … & Beal, M. F. (1999). Age-dependent increases in oxidative damage to DNA, lipids, and proteins in human skeletal muscle. Free Radical Biology and Medicine, 26(3-4), 303-308.

[5] Brown, C. N., & Bayer, K. U. (2024). Studying CaMKII: tools and standards. Cell reports, 43(4).

Date Posted: September 9, 2026

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Comparing the Responsiveness of Epigenetic Aging Biomarkers

In a recent study, researchers have evaluated how responsive several DNA methylation (DNAm) biomarkers are to a range of longevity interventions [1].

Waiting too long

Testing lifespan-extending interventions in humans has a major problem: it can take many years, or even decades, to see results. Nobody wants to wait that long. Therefore, it is essential to find proxies, such as biomarkers, that accurately reflect whether an intervention is working. Some of the most popular biomarkers in the aging field are epigenetic aging clocks, DNAm biomarkers that are intended to reflect a person’s biological age or rate of aging.

While these clocks are becoming increasingly popular, they are still not sufficiently validated to serve as surrogate endpoints for human longevity clinical trials, and there isn’t enough data on their responsiveness to longevity-promoting interventions.

“If these new biomarkers are eventually validated to predict long-term health, scientists will be able to evaluate anti-aging therapies much faster,” said Raghav Sehgal, the lead author of this study. “Instead of waiting decades for evidence from clinical trials, we’ll be able to see which interventions are effective and in which people in a few years or even months.”

Multiple comparisons

To analyze how epigenetic aging clocks and other biomarkers respond to various aging interventions, the researchers used data from 51 existing longitudinal interventional studies. The researchers grouped the interventions in their dataset into four groups: “lifestyle (including diet and exercise), pharmacological (for example, metformin, rapamycin, semaglutide, ketamine and anti-TNF therapy), supplements (for example, omega-3 fatty acids and folate) and medical procedures (for example, hyperbaric oxygen therapy, organ transplants and gene therapy).”

Then, they calculated the effect of each intervention using 16 epigenetic clocks and 94 other DNA methylation biomarkers; they used ‘DNAm biomarkers’ as an umbrella term for both of those tools.

Using multiple biomarkers can serve two functions. First, surrogate biomarkers can help predict long-term outcomes. Second, discovery biomarkers can help explain which molecular mechanisms an intervention affects [2, 3].

“What we did was pretty unique,” Sehgal said. “We already know that certain things might prolong healthspan and lifespan. There are data from retrospective analyses as well as animal models. We took all that knowledge along with the real-world clinical studies to identify which interventions in humans were slowing down aging across the board in these known biomarkers.”

Comparing multiple interventions using multiple biomarkers allowed the authors to identify patterns in how different intervention types affect health and aging. For example, they noted that pharmacological interventions produced stronger DNAm biomarker responses than any other category and were the only ones with significantly larger effect sizes. They were also one of two categories, along with a lifestyle intervention, to show significantly reduced epigenetic age. The authors hypothesize that pharmacological interventions’ robust effects may stem from their ability to target inflammation and metabolic pathways such as TNF, AMPK, and mTOR.

Replications matter

The authors note that their compiled studies include replicated studies of the same intervention and use multiple clocks to measure similar outcomes, which allows them to test whether certain interventions have consistent effects.

To identify intervention types with a strong, consistent effect on biomarkers, the authors propose two requirements: “the intervention should modify DNAm biomarkers of a given generation to the same magnitude and direction in a particular study” and “a second study of the same intervention should modify the same biomarkers.”

Both requirements were met by therapies that reduce tumor necrosis factor (TNF) and are used to treat conditions such as inflammatory arthritis and inflammatory bowel disease, suggesting that such therapies may prevent pathological aging in patients with autoimmune disorders. The requirements were also met by two different types of Mediterranean diets in healthy populations.

Not all DNAm biomarkers are created equal

Tests of responsiveness and concordance of the DNAm biomarkers, defined as ”the likelihood that if a DNAm biomarker detected a significant effect, then others would agree on the effect”, showed the superiority of generation 2+ biomarkers.

Similarly, biomarkers differed in sensitivity. Focusing on lifestyle and pharmacological interventions, the researchers noted intervention-type-specific sensitivity across multiple biomarkers and differences in effect-size magnitude between categories: DunedinPACE was highly responsive in the lifestyle category, but in the pharmacological category, it was affected by fewer interventions than other second-generation biomarkers.

Study population health status also affected DNAm biomarker responses, with several biomarkers significantly more responsive in disease groups than in healthy populations, similar to previous studies suggesting that people with health problems may have more room for improvement than healthy people [4, 5]. Only DunedinPACE showed similar response levels in both populations, suggesting that it can be applied in both contexts.

The authors suggest that the training population on which those biomarkers were developed partly explains these observations, since biomarkers trained on populations with more diverse health statuses are more sensitive to changes in populations with disease, while those trained on healthier groups have higher sensitivity in healthier cohorts.

Understanding biology

Those researchers also went a step further, using Generation X (GenX) DNAm biomarkers to gain mechanistic insights into biological aging, which can later support more precise, targeted aging therapies. With this technique, the authors observed which organs are affected by different interventions, such as a reduction in lung system scores upon smoking cessation or the impact of metformin on inflammatory, brain-related, and metabolic pathways, as well as the effect of different diets on various biomarkers and scores, which can aid in measuring diet-specific impacts on different aspects of aging.

Such analyses let researchers focus on biomarkers specific to certain pathways, capturing earlier changes in those systems and organs that composite biomarkers can miss by “averaging out” effects across components.

Narrowing down the choices

In summary, understanding which DNAm biomarkers work best and provide the most useful information across different interventions helps researchers choose the best tools for future clinical trials, minimizing time and cost while maximizing meaningful results.

This analysis of DNAm biomarkers suggests that clinical trials should prioritize generation 2+ clocks, mainly DunedinPACE and PCGrimAge, since their responses were the strongest and the most consistent. However, they still need validation as surrogate endpoints in human clinical trials.

“As researchers, we have a long way to go in understanding the aging process and whether the steps we take to manage it really work,” said Sehgal.

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Literature

[1] Sehgal, R., Borrus, D., Armstrong, J. F., Gonzalez, J., Kasamoto, J., Markov, Y., Priyanka, A., Smith, R., Carreras-Gallo, N., Lasky-Su, J., Dwaraka, V. B., Corley, M. J., & Higgins-Chen, A. (2026). Responsiveness of epigenetic aging biomarkers to longevity interventions in humans. Nature medicine, 10.1038/s41591-026-04562-9. Advance online publication.

[2] Moqri, M., Herzog, C., Poganik, J. R., Biomarkers of Aging Consortium, Justice, J., Belsky, D. W., Higgins-Chen, A., Moskalev, A., Fuellen, G., Cohen, A. A., Bautmans, I., Widschwendter, M., Ding, J., Fleming, A., Mannick, J., Han, J. J., Zhavoronkov, A., Barzilai, N., Kaeberlein, M., Cummings, S., … Gladyshev, V. N. (2023). Biomarkers of aging for the identification and evaluation of longevity interventions. Cell, 186(18), 3758–3775.

[3] Fleming, T. R., & Powers, J. H. (2012). Biomarkers and surrogate endpoints in clinical trials. Statistics in medicine, 31(25), 2973–2984.

[4] Yao, A., Gao, L., Zhang, J., Cheng, J. M., & Kim, D. H. (2024). Frailty as an Effect Modifier in Randomized Controlled Trials: A Systematic Review. Journal of general internal medicine, 39(8), 1452–1473.

[5] Pandey, A., Kitzman, D. W., Nelson, M. B., Pastva, A. M., Duncan, P., Whellan, D. J., Mentz, R. J., Chen, H., Upadhya, B., & Reeves, G. R. (2023). Frailty and Effects of a Multidomain Physical Rehabilitation Intervention Among Older Patients Hospitalized for Acute Heart Failure: A Secondary Analysis of a Randomized Clinical Trial. JAMA cardiology, 8(2), 167–176.

Date Posted: September 8, 2026

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Late-Life GLP-1 Treatment Increases Lifespan in Female Mice

In a new study, semaglutide given late in life increased median lifespan in female mice by more than 12% and improved various health markers. Semaglutide’s effect possibly went beyond caloric restriction [1].

Old mice, new drugs

GLP-1 receptor agonists, which act on a hormone that regulates insulin secretion and appetite, have revolutionized obesity treatment, showing benefits across several seemingly unrelated diseases. This raised the question whether the drugs’ effect goes beyond caloric restriction, which itself is a potent anti-aging intervention that has produced robust healthspan and lifespan extensions in animal models [2]. So far, human studies have not yielded conclusive results [3], so there is value in going back to animal studies, where interventions can be investigated across the model’s entire lifespan.

A new study, led by scientists from UC Berkeley and published in Nature, features a fairly straightforward design: take female mice, start giving them GLP-1 receptor agonists late in life, and see what happens. The researchers began daily semaglutide treatment in 20-month-old, non-obese, non-diabetic, female mice that ate standard lab chow, and continued it for the rest of their lives. Forty mice received semaglutide, and 39 received saline injections.

Median lifespan extended

Semaglutide reduced food intake by approximately 24% and lowered body weight. Body composition shifted toward a lower fat percentage and a higher lean-mass percentage. This, however, does not mean that overall lean mass increased – just that the animals lost more fat than muscle. There was no significant change in energy expenditure, suggesting that weight loss was mainly due to reduced calorie intake.

In the central result, median lifespan increased from 742 to 834 days: a gain of 92 days, or approximately 12.4%. The controls’ median lifespan amounted to 24.4 months, which means that although the treatment period was fairly short, it nevertheless produced a significant increase in lifespan. 742 days is also on the lower end of female C57BL/6 mice’s lifespan in previous studies, so replicating the results in longer-lived cohorts would be valuable. Mortality was delayed across several non-tumor categories, which is consistent with benefits extending beyond one particular terminal condition.

Live long – but how about prospering?

To determine if the longer-lived animals were also functioning better, the researchers treated old mice in a separate cohort for three months, testing movement, exploration, memory, physical performance, and glucose regulation. Most functional comparisons involved ten mice per group.

Semaglutide-treated mice moved more and explored exposed areas more readily in unfamiliar environments. They also performed better in a spatial memory test. Motor coordination, hanging performance, and treadmill endurance all improved, as did glucose tolerance.

The researchers then analyzed various aging-related cellular processes. Hematopoietic stem cells (HSCs) age somewhat paradoxically: they can become more numerous even as their regenerative performance deteriorates. They also increasingly favor the myeloid lineage, which includes monocytes and granulocytes, over the lymphoid lineage, which includes B and T cells. Semaglutide treatment partially reversed these aspects of HSC aging.

In the dentate gyrus, a region of the hippocampus involved in learning and memory, semaglutide increased the number of both dividing cells and immature neurons, suggesting improved neurogenesis and providing a plausible biological link to the uptick in memory performance.

Inflammation is a major hallmark of aging. Semaglutide reduced inflammatory gene expression in liver and muscle tissues and reduced inflammatory immune-cell signals in the liver. This included fewer macrophages expressing high levels of the inflammatory cytokine IL-6.

Several markers associated with cellular senescence also decreased after treatment, including expression of p16 and p21 in the liver, visceral fat, and spleen along with senescence-associated β-galactosidase staining in the kidney and spleen. However, this does not establish that semaglutide has a senolytic effect.

In the liver and spleen, semaglutide reduced the proportion of cells that bear γ-H2AX, a marker associated with DNA damage. It also increased mitochondrial gene expression and ATP content in muscle and reduced mitochondrial oxidant signaling in blood stem cells. On top of that, the treatment seemed to improve some markers of cellular stress triggered by misfolded proteins.

More than eating less?

To understand how much of the effect could be explained simply by mice eating less, the team compared semaglutide directly with a 24% reduction in food intake in another cohort of old female mice. In an experiment that lasted for five months, ten animals per group received saline, semaglutide, or caloric restriction.

The two interventions resulted in similar total food intake and comparable weight and fat loss, but the mice exhibited different eating patterns: mice under caloric restriction finished their daily rations quickly and then fasted for a prolonged period. Semaglutide-treated mice ate more gradually throughout the day, consistent with a suppressed appetite rather than enforced restriction.

Both treatments broadly preserved physical function, while untreated animals declined. The similarities spanned movement in unfamiliar environments, rotarod and hanging performance, and treadmill endurance.

However, semaglutide-fed mice fared better than calorically restricted ones in spatial memory and glucose tolerance. Here, semaglutide improved performance above baseline, while caloric restriction generally maintained it near baseline. However, there was no caloric-restricted lifespan group, so this study did not answer the question of whether semaglutide extended life more than an equivalent reduction in food intake would have done.

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Literature

[1] Feng, Y., Barthez, M., Wang, Y., Chen, Y., Qiu, H., Wang, C. L., … & Chen, D. (2026). Late-life semaglutide treatment slows ageing and extends lifespan in female mice Nature, 1-8.

[2] Mattison, J. A., Colman, R. J., Beasley, T. M., Allison, D. B., Kemnitz, J. W., Roth, G. S., … & Anderson, R. M. (2017). Caloric restriction improves health and survival of rhesus monkeys. Nature communications, 8(1), 14063.

[3] Newsome, P., Francque, S., Harrison, S., Ratziu, V., Van Gaal, L., Calanna, S., … & Sanyal, A. (2019). Effect of semaglutide on liver enzymes and markers of inflammation in subjects with type 2 diabetes and/or obesity. Alimentary pharmacology & therapeutics, 50(2), 193-203.

Date Posted: September 7, 2026

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Mice With Growth Hormone Halted in Middle Age Live Longer

Researchers publishing in Aging Cell have described how stopping growth hormone receptor production in midlife significantly lengthens the lives of mice.

Growth but diabetes

Growth hormone affects the metabolism of fats (lipids), increasing the levels of circulating fatty acids while increasing insulin-like growth factor 1 (IGF-1) and impairing the function of insulin itself [1]. Growth hormone has been associated with tissue-specific forms of aging [2], and people who are congenitally insensitive to growth hormone (Laron syndrome) exhibit increased resistance to multiple aspects of aging, including diabetes, cognitive decline, and cardiovascular problems [3].

This relationship between growth hormone and aging is similar in mice and people [4]. Mice with reduced levels of growth hormone live longer than their unaltered counterparts [5], and such mice also have significant reductions in debilitating age-related conditions, such as osteoarthritis [6].

Those mouse models, however, are genetically modified, with effects from birth. Bringing this into the clinic requires affecting growth hormone in adulthood in order to avoid interfering with growth and development. This team has previously developed a mouse model in which growth hormone is disrupted in young adulthood, finding that such mice live longer than wild-type mice [7].

In this study, the researchers built on their previous findings by using a mouse model that ceases production (knockout) of the growth hormone receptor (GHR) at 12 months of age, which roughly corresponds to midlife in humans: a time during which many people would presumably begin to seek treatment for age-related disorders.

The longest-lived mice live even longer

The very first result that the researchers discuss is lifespan, which was markedly improved in both males and females. While they were shorter and smaller than their unaltered counterparts later in life, GHR knockout males had an improved survival curve compared to the male control group. Females with GHR knocked out had no changes in body weight or size but also an improved survival curve.

Interestingly, this lifespan increase was found predominantly in the longest-lived animals, particularly in females; while the shortest-lived members of both the control and GHR knockout groups died at roughly the same ages, the longest-lived female GHR knockout mice lived for four months longer than the longest-lived female control mice. This increase in lifespan occurred alongside significant reductions in IGF-1, particularly in males.

Under normal circumstances, an increase in fat mass and a decrease in lean mass is a cause for concern, and treatments that improve healthspan metrics in mice often do the exact opposite. With a GHR knockout, however, both sexes had increased fat mass and decreased lean mass in later life compared to the control group. Despite this induced obesity and reduction in muscle mass, inflammatory biomarkers were largely unaffected, the mice were not weaker overall according to physical performance tests, and males in the GHR knockout group had improved insulin responses and less fasting glucose; females were unaffected in this area.

Tissue-specific effects

The porous parts of the spinal bones (vertebral trabecular bone) were significantly preserved in male mice, with porosity and bone mineral density being more like that of younger mice. Females were unaffected in this area.

The liver responds strongly to growth hormone signaling, so it is unsurprising that its gene expression was significantly changed when GHR was knocked out, with males being more strongly affected than females. Interestingly, the livers of male mice began exhibiting gene expression that was more associated with that of female mice, and even female mice with GHR knocked out had reduced expressions of genes that are more strongly expressed in males.

Near the end of this paper, the researchers express the opinion that “these findings reinforce the central role of the GH/IGF-1 axis in aging biology and support the concept that pharmacological inhibition of GH signaling during adulthood may represent a feasible strategy for promoting healthy aging.” They reaffirm their findings in a short communication sent to Aging Cell, in which they note the multiple potential problems with completely restricting growth hormone and focus on growth hormone antagonism as a potential treatment avenue.

There is already such an antagonist that has been approved by the FDA, Pegvisomant, which has never been clinically tested for any potential anti-aging effects, despite proposals having been made to do so [8]. While this research provides evidence for the potential of such a trial, it may also be the case that treatments that impact growth hormone at a tissue-specific level can provide tangible lifespan and healthspan increases in people, although substantial work needs to be done in development and trials in order to confirm this.

Yes I will donate❤️

Literature

[1] Vijayakumar, A., Novosyadlyy, R., Wu, Y., Yakar, S., & LeRoith, D. (2010). Biological effects of growth hormone on carbohydrate and lipid metabolism. Growth Hormone & IGF Research, 20(1), 1-7.

[2] Chesnokova, V., Zonis, S., Ainsworth, R., Apaydin, T., Valencia, C. W., Greiner, E. C., … & Melmed, S. (2025). Local Growth Hormone Facilitates Aging of the Colon Epithelial Microenvironment. Aging Cell, 24(10), e70187.

[3] Guevara-Aguirre, J., Mishra, A., Canepa, M., Guevara, C., Villacres, Á., Guevara, A., … & Longo, V. D. (2024). Normal or improved cardiovascular risk factors in IGF-I-deficient adults with growth hormone receptor deficiency. Med, 5(7), 816-825.

[4] Qian, Y., Berryman, D. E., Basu, R., List, E. O., Okada, S., Young, J. A., … & Kopchick, J. J. (2022). Mice with gene alterations in the GH and IGF family. Pituitary, 25(1), 1-51.

[5] Bartke, A., & Darcy, J. (2017). GH and ageing: Pitfalls and new insights. Best Practice & Research Clinical Endocrinology & Metabolism, 31(1), 113-125.

[6] Liu, H., Davis, T., Duran-Ortiz, S., Martino, T., Erdely, A., Profio, S., … & Zhu, S. (2024). Growth hormone-receptor disruption in mice reduces osteoarthritis and chondrocyte hypertrophy. Geroscience, 46(5), 4895-4908.

[7] Duran‐Ortiz, S., List, E. O., Ikeno, Y., Young, J., Basu, R., Bell, S., … & Kopchick, J. J. (2021). Growth hormone receptor gene disruption in mature‐adult mice improves male insulin sensitivity and extends female lifespan. Aging cell, 20(12), e13506.

[8] Longo, V. D., Antebi, A., Bartke, A., Barzilai, N., Brown‐Borg, H. M., Caruso, C., … & Fontana, L. (2015). Interventions to slow aging in humans: are we ready?. Aging cell, 14(4), 497-510.

Date Posted: September 3, 2026

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The Last Generation to Die: Interview With Tim Maupin

Filmmaker Tim Maupin has spent a number of years developing The Last Generation to Die, a near-future film about what happens when the first true rejuvenation technologies arrive and who gets left behind. The project has now reached the top 65 of the Future Vision XPrize, a global contest seeking optimistic visions of humanity’s future. We talked to him about the personal stakes behind the story, the challenge of creating future positive stories, and why the film’s central dilemma feels increasingly urgent.

Thanks for joining us, Tim. So, the exciting news is that one of your films was nominated for the Future Vision XPrize. The brief for the contest is to create a 3-minute sci-fi trailer depicting an optimistic, abundant future for humanity. The grand prize winner gets $2.6M+ to turn their vision into a feature film, plus over $1M in prizes for runners-up. Can you tell us a little bit about that, Tim?

Yes, it’s a longevity-focused film that I’ve been working on for quite a while called The Last Generation to Die. It is in the top 65 of over 2500 entries in the X Prize Future Vision contest, which is definitely exciting news.

That’s great, I remember watching the preview some years ago, and I always thought it was a really interesting idea, so I’m really glad to see that it has been nominated. Making it into the top 65 films is a real achievement, so what happens next?

The next step is they choose the top ten, and then that goes down to the top five. The top five get to go to the moonshots event, which is a pretty big deal. The judges are Neil deGrasse Tyson, Mira Lane, Neil Stevenson, and Rod Roddenberry. So, there are some important names involved with this. From there you pitch live, and they show the trailers, and then they actually choose the winner live that night in the room.

It’s a really important event, so fingers crossed, and we’ll see where it goes from there. I think the top ten also get invited to the event too, so even getting into the top ten would be pretty great as well.

Sounds good, so can you tell us a little more about the film itself?

I made it as a short film a few years ago that was played at some film festivals. I’d always envisioned it as a feature, but I really got back into that process after my father passed away in 2019. That was when I went back to the script, and, in some ways, I became a lot more able to write it, because I was living the material in a way that I hadn’t before. After that, it became a lot more real and still is. My mom is also aging, and I’m seeing that very directly, so it’s a very personal and real film.

It’s set in the near future where a female scientist named Lily is at the forefront of a new technology that’s going to slow and even reverse aging. Her father Oliver has a major heart issue, and she’s able to get him on the trial for this technology as a last-ditch effort to save him. And it works and I mean it works really well, he actually starts de-aging and gets much healthier at the same time.

During the film, Lily’s mother falls ill with a rare neurodegenerative disease. But, she doesn’t fit the inclusion criteria of the trial, and they are too afraid to risk trying the technology on her, so her mother’s health ends up failing while her father’s health actually improves because his age is reversing.

So, you have this interesting dynamic between her parents as the film goes on. From a longevity standpoint, I think it is a great thought experiment to consider what would happen in terms of our current form of aging and what could happen with some kind of new rejuvenation technology. I hope that it pulls on the heartstrings of folks in a very direct way as events play out like that.

Then, there’s a whole extra plot that covers how some people in the company are trying to maximize profits with this technology, and she’s fighting that as well. Ultimately, I’d say it’s a bittersweet film, it’s very positive in one way but also very real and nuanced in another.

From my perspective, I think setting a film at the gulf between these two worlds, situations like this will happen. There’ll be a point where some people unfortunately don’t make it and some people get age-reversal technologies. I just think that’s a great point to set the film because it’s got inherent conflict from that standpoint, and you get to see those two dynamics in one spot in time.

That’s basically what the film’s about. I hope by seeing that it encourages people to want to bring this technology on faster and do what they can to support it.

That’s a good synopsis. I saw the original trailer, and I always thought it was an intriguing idea. So glad to see it’s reached this stage, and, obviously, I’ve got my fingers crossed that it makes the top five because it’s exploring some very important near-future possibilities.

The dynamic in the film between the parent who qualifies for the trial and the one who doesn’t feels especially timely. With the first biomedical repair therapies now entering human trials, questions about access and how we regulate multi-disease approaches are becoming real rather than theoretical.

So, let’s talk about how the film originally got started. I understand that it has roots with our organization, Lifespan.io, as it was called back then when the film started. Can you tell us a little bit about how that came about and how it helped to get the film underway?

Yes, absolutely. I started working for Lifespan.io around the same time that I got back into the film, which was great timing because I was surrounded by folks who are working on the same goal and seeing the actual reporting on the research helped to inform the film. So, being involved with Lifespan.io at the time was informative for the film but also energizing on a personal level.

Not only that, but Keith Comito and Oliver Medvedik from Lifespan.io actually served as advisors for the film too. Lifespan.io also helped get the film off the ground by acting as a fiscal sponsor in those early days.

Talking about actually keeping the film going and getting it to where it is, specifically, let’s talk about the jellyfish connection. Can you tell us a little bit about jellyfish and how it has helped you to get the film to where it is?

Jellyfish is a related organization to Lifespan in some ways and includes Keith Comito. The idea behind it was to build a community of filmmakers and artists focused on longevity-related film and media. Films that were a little bit more of the positive future side of things. The goal for the past couple of years has been to try to support that community and find ways to help fund these projects. Funding for films, especially independent films, is always challenging, and so the Jellyfish DAO was started as a crypto model.

But, we are looking at ways to expand that beyond just crypto funding and looking for unique and innovative funding models that might help to grow and support longevity-related films. It’s also a good test case for decentralized science to do things that public funding probably wouldn’t support.

To speak more broadly about the concept of the prize itself, all the films in the competition appear to have a future-positive focus, this is the opposite of what a lot of films set in the future have, which instead often have dystopian storylines. What are your thoughts on that?

The dystopian versus positive storytelling is always an interesting thing to consider, and I agree that dystopian tales do have their place. I think it’s a good simulation, as it were, to imagine how things could go.

But, I strongly agree with the premise of the contest. We do have a lot of dystopian tales, arguably too many, and I think it’s time to balance things in the other direction a bit. Because some might argue that we are living in a bit of a dark time right now and I think we do need to be projecting positive visions to counter that. It’s also very clear that movies and culture do actually shape how things happen to a certain degree in the future.

So, I think by continuing to project positive things, we’re continuing to push forward towards a better future. Even if it may seem like it’s just a movie, I honestly believe that it filters through people’s psyche and does actually change how things can go. I’m honestly very grateful that they’ve put this contest out because I think it’s a much needed counterbalance.

But, I will admit it’s not easy to make future positive films. Dystopian films are easier to write and make because there’s a clear villain and there’s more obvious conflict. It is a challenge to come up with something that still has conflict, still engages people, but ultimately ends in a positive place. It’s been really interesting to see the other creators in the contest try to figure that out as well.

I definitely think it’s a worthy challenge and something worth pushing for. Future positive framing is also important for the biomedical repair field too, because the field does have a tendency to overpromise and underdeliver, which has given it a somewhat tarnished image. There’s a lot of misinformation, hype, and also misunderstanding about what the field is really doing – treating age-related diseases by treating the reasons we age and get sick in the first place. Do you think films like this can probably help with that image?

I think so, and I would say that my film takes a fairly nuanced approach that isn’t as grandiose as immortality or anything like that. It’s taking a more realistic look at some of the more commonly overlooked things about the field. Concepts that make a ton of sense, like if you target aging, you’re simultaneously combating many diseases at once. A film like this can put that in a way that makes sense in a story fashion where it’s not just didactic information that you’re sort of preaching to people.

So yes, I would agree, and there’s also other narratives like the concern that only the billionaires are going to get this tech, which I’m not saying isn’t worth thinking about as a potential risk, but it’s also pushing towards the idea that this really should be for everyone as a counterpoint and that’s actually possible if we decide to make it so. So, I think having the vision to move in a positive direction is important, especially in a movie form.

What sort of impact do you think the film might have if it gets nominated in the top five?

Great question! If it reaches that point, from what I’ve heard, being in the top five gives you more exposure, because you’re on the stage and Range Media Partners and others are right there. So I think it would stand a good chance of getting a lot more attention and potentially some funding.

The other thing to mention is that we have an amazing cast. We have Ed Harris, Lily Rabe and Mamoudou Athie on board now. That’s quite something for an independent film, it’s an achievement to have such great actors interested and I think they could also help to potentially speed that up.

Ideally, we’d be moving a lot closer to getting it into production if we got into the top five. The ideal production window would be next year in spring or summer. So, being in the top five in the contest would absolutely help speed that up.

Wow, that’s quite an upgrade from the original trailer I watched a few years ago, then. Where can people watch the contest version?

People can watch The Last Generation to Die contest video over at the FutureVision XPrize and also vote for it and any of the other films in the contest. They have a pretty cool voting platform where it’s not just a social media-based contest. They give you two trailers, and you vote for one and you cycle through. It’s a little cooler than what you usually see for these things, so I would encourage people to go check those out and vote.

Jellyfish has another film in there called Senti. I would encourage everyone to go take a look at the films there and support this prize because I think we need more of it, and it sounds like they’re gonna continue to do it.

That sounds great. Do we know exactly when they’ll announce the finalists?

I think next week, we will find out the top 10, so it’s very soon. Then I think the top five may come the week after that. So within the next two weeks, we’ll probably find out the top five.

Thank you for taking the time to speak with us today, Tim, and we wish you the best of luck with your film.

As The Last Generation to Die makes clear, the arrival of the first biomedical repair therapies in human trials brings questions of access and equity into sharp focus. Ensuring these technologies benefit society broadly, rather than becoming another driver of inequality, is not only a moral issue but an economic one, something we explore in more detail in our recent white paper – Why Democratizing Rejuvenation Is an Economic Imperative.

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That’s great, I remember watching the preview some years ago, and I always thought it was a really interesting idea, so I’m really glad to see that it has been nominated. Making it into the top 65 films is a real achievement, so what happens next?

Sounds good, so can you tell us a little more about the film itself?

That’s a good synopsis. I saw the original trailer, and I always thought it was an intriguing idea. So glad to see it’s reached this stage, and, obviously, I’ve got my fingers crossed that it makes the top five because it’s exploring some very important near-future possibilities.

So, let’s talk about how the film originally got started. I understand that it has roots with our organization, Lifespan.io, as it was called back then when the film started. Can you tell us a little bit about how that came about and how it helped to get the film underway?

Talking about actually keeping the film going and getting it to where it is, specifically, let’s talk about the jellyfish connection. Can you tell us a little bit about jellyfish and how it has helped you to get the film to where it is?

To speak more broadly about the concept of the prize itself, all the films in the competition appear to have a future-positive focus, this is the opposite of what a lot of films set in the future have, which instead often have dystopian storylines. What are your thoughts on that?

What sort of impact do you think the film might have if it gets nominated in the top five?

Wow, that’s quite an upgrade from the original trailer I watched a few years ago, then. Where can people watch the contest version?

That sounds great. Do we know exactly when they’ll announce the finalists?

Thank you for taking the time to speak with us today, Tim, and we wish you the best of luck with your film.

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