Alongside Müller, Lora K. Heisler from the University of Aberdeen, Randy J. Seeley from the University of Michigan, and Brian Finan from Eli Lilly and Company were honored with the 2026 Gill Transformative Investigator Award.  

New Therapeutic Approaches for Obesity and Diabetes

Müller’s research has made an important contribution to improving our understanding of the biological mechanisms underlying obesity and diabetes. His work has provided key insights into GIP receptor biology in the central nervous system and contributed to the development of a new generation of incretin-based polyagonists.

These compounds activate several receptors simultaneously and can therefore influence different metabolic processes, including the regulation of blood glucose, appetite and body weight. The concept of polyagonists was originally developed by Matthias Tschöp and Richard DiMarchi and was subsequently further advanced, among others, by Müller and his team at Helmholtz Munich from a biological and mechanistic perspective.

More recent work by Müller and his team takes this concept one step further. They are investigating how incretin-based molecules can not only combine several metabolic signals, but also selectively deliver additional therapeutic components to specific cells. The aim is to develop new and even more precise approaches for the treatment of obesity and type 2 diabetes.

At the Gill Symposium, Müller presented his research in a talk entitled “From Novel Insights into Energy Metabolism Control by GIPR Agonism to New Therapies for Obesity and Diabetes”.

A Special Connection to Munich

Müller’s award also continues a special connection between metabolic research in Munich and the Gill Awards. Following Matthias Tschöp, Müller is the second scientist from a German research institution to receive a Gill distinction. Tschöp received the Gill Distinguished Scientist Award in 2014 while affiliated with the Technical University of Munich. He later served as Scientific Managing Director of Helmholtz Munich.

The Gill Transformative Investigator Award thus recognizes Müller’s long-standing contribution to a field of research that has fundamentally expanded the possibilities for treating obesity and type 2 diabetes in recent years.

Health Effects from Heat, Cold & Air Pollution

Several findings concerned the health effects of heat and air pollution. Research presented at the conference estimated that heat was associated with around 145,000 work-related injuries per year across the countries studied, while cold was associated with around 82,000. The analysis used data collected up to 2023 and was particularly relevant in the context of the heatwaves experienced in Europe in 2026.

A study based on data from the German National Cohort, NAKO, reported around 30% more cardiometabolic multimorbidity among people living in highly polluted urban environments compared with those living in areas with low exposure. The study by Helmholtz Munich PhD researcher Asmaa Alselwi received one of the conference’s awards for students and early-career researchers.

Plastics and Cardiovascular Health

Plastics formed another focus of the conference. Researchers discussed possible direct health effects of micro- and nanoplastics as well as indirect effects, such as discarded plastic providing breeding sites for insects that transmit disease.

A systematic review by Dr. Fiona Niedermayer of Helmholtz Munich identified 31 studies on associations between endocrine-disrupting chemicals and cardiovascular disease. Across these studies, phthalate exposure was consistently associated with cardiovascular mortality.

The Environmental Footprint of Artificial Intelligence

The conference also examined the environmental footprint of digital technologies. Prof. Francesca Dominici of Harvard University presented research on the potential use of artificial intelligence to assess local climate and health risks.
Her presentation also included estimates of the environmental footprint of large data centers in the United States, including annual electricity use of 68 to 99 terawatt-hours, around 45 million tons of carbon dioxide emissions and approximately 300 billion liters of water use. These findings raised questions about how the environmental and health effects of AI infrastructure can be assessed.

Press Conference at the Deutsches Museum

On 3 September, researchers discussed selected conference findings with journalists at a press conference at the Deutsches Museum, held in connection with its Planetary Health exhibition. Participants from ISEE, Helmholtz Munich, universities and the World Health Organization covered topics including air pollution and respiratory infections in children, pesticides and Parkinson’s disease, and the use of scientific evidence in public health policy.

A nationwide study of more than one million children in Denmark, for example, reported an association between higher air pollution exposure and serious respiratory infections from infancy through adolescence, even at comparatively low pollution levels.

From Research to Public Health Guidance

The WHO contribution described how scientific evidence informs public health guidance. The WHO Air Quality Guidelines, which draw on systematic reviews of around 500 scientific papers, served as a reference for the revision of the EU Ambient Air Quality Directive adopted in 2024.

The conference and press briefing provided an overview of current environmental health research and its relevance for prevention and evidence-informed policy development.

Watch the Full Press Conference

A recording of the full press conference is available here: ISEE2026 Press Conference - Environmental Epidemiology in a Changing World.

Idiopathic pulmonary fibrosis (IPF) is a severe and currently incurable lung disease characterized by progressive scarring of the lungs. Disease progression varies widely between patients, making it difficult to predict outcomes and tailor treatment strategies. Understanding the factors that drive rapid progression remains one of the most important challenges in the field.

Analyzing samples from patients with IPF, the research team found evidence of clonal hematopoiesis in 38 percent of cases. Patients carrying these mutations were significantly more likely to experience rapid disease progression compared with patients without the mutations. They also showed a substantially greater decline in lung function over a 12-month period.

First author Lori Asarian would like to thank all patients who participated in the study: “Their contribution was essential to uncover this connection that may have important implications for patients with IPF.”

Clonal hematopoiesis - a blood-based indicator of IPF progression?

The findings give new insights into how age-related changes in the hematopoietic system may influence lung fibrosis. "The study highlights the importance of looking beyond the lung itself to better understand disease mechanisms," says Isis Fernandez, group leader at LHI. "Our findings strengthen the link between age-related blood cell changes and pulmonary fibrosis and may help improve patient stratification in the future."

The study further reinforces the Institute of Lung Health and Immunity's leading expertise in pulmonary fibrosis research. Through close collaboration with clinical partners, LHI researchers are working to better understand the biological mechanisms underlying this devastating disease and to identify biomarkers that could support earlier intervention and more personalized treatment approaches.

Publication:

Asarian L. et al. Clonal hematopoiesis is associated with disease progression in idiopathic pulmonary fibrosis. JCI Insight. 2026

Read the full paper:  https://insight.jci.org/articles/view/198458

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Oktober 2026
Reason for procurement/Produkt:    Image-basierte Plattform zur Dokumentation der Monoklonalität von 
                                                         CRISPR/Cas- editierten iPSC-Linien  
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Bau-Vergabestelle / construction contracting authority
Einkauf und Materialwirtschaft/Purchasing
(Geb./building 11)
Tel:      089-3187-2138
Email: frank.georgi@helmholtz-munich.de

Bekanntmachung

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Early detection can offer significant benefits. When children with early-stage type 1 diabetes are identified and monitored regularly, the risk of diabetic ketoacidosis (DKA) at clinical onset can be substantially reduced. The onset of diabetes may then be less severe, and insulin treatment can be started promptly, often on an outpatient basis. Early diagnosis also gives families time to prepare for living with the condition and its treatment.

In addition, identifying type 1 diabetes before symptoms appear creates an opportunity to consider disease-modifying therapies at an appropriate stage and potentially delay the clinical onset of the disease.

The Majority of Children Who Develop Type 1 Diabetes Have No Family History

Screening people from families already known to be at high risk is not enough: more than 85 per cent of people newly diagnosed with type 1 diabetes have no family history of the condition. Moreover, once islet autoantibodies have been confirmed, the disease progresses at a similar rate regardless of family history.

The consensus recommends an initial screening between the ages of two and four years. If no islet autoantibodies are detected, further screening should take place between the ages of six and eight and again between the ages of 10 and 15. Studies show that islet autoantibodies first appear particularly frequently during these stages of childhood.

Within these age ranges, the timing of screening can be adapted to existing national or regional screening programmes. The recommendations also allow for a phased introduction: depending on local circumstances, programmes could initially focus on children at increased risk before being expanded to the wider population.

“With this international consensus, we have established a common framework for how population-wide screening for type 1 diabetes can be implemented in practice,” says Prof. Anette-Gabriele Ziegler, Director of the Institute for Diabetes Research at Helmholtz Munich and lead author of the consensus paper. “The diagnosis of early-stage diabetes is a step-by-step process: it begins with a sensitive screening test and is confirmed by highly specific second-line tests and a second blood sample. The specific design of the screening programme should be adapted to the respective healthcare system and, where possible, linked to existing screening programmes.”

Clear Communication and Support Are Essential

A confirmed diagnosis should be communicated to families in person and in a clear and empathetic manner. Psychosocial support should also be available when needed.

Separate international consensus recommendations already provide guidance on the regular monitoring of people diagnosed with early-stage type 1 diabetes.

The new recommendations have received broad international support. A total of 20 professional and patient organisations endorse the consensus paper, including the European Association for the Study of Diabetes (EASD), the International Society for Paediatric and Adolescent Diabetes (ISPAD) and the International Diabetes Federation Europe (IDF Europe).

Original Publication

Ziegler et al., 2026: International consensus guidance for general population screening for islet autoantibodies to diagnose early‑stage type 1 diabetes: a nominal group technique process, Diabetologia. DOI: 10.1007/s00125-026-06841-z

The visit began with an introduction to Helmholtz Munich and its scientific mission by Dr. Michael Frieser. Administrative Managing Director, followed by an overview of HI-MAG’s research activities presented by institute director Prof. Matthias Blüher.

HI-MAG is a joint initiative of Helmholtz Munich, Leipzig University and University of Leipzig Medical Center. Its research focuses on understanding how adipose tissue dysfunction leads to metabolic and vascular diseases. Through its translational bench-to-bedside approach, HI-MAG combines fundamental research with clinical studies across all stages of life. The institute’s goal is not only to develop new therapeutic concepts for people living with obesity but also to identify opportunities for prevention early in life.

“HI-MAG demonstrates the great value of strong scientific partnerships. Together with Leipzig University and University of Leipzig Medical Center, we are able to advance outstanding research that addresses major health challenges and creates new opportunities for prevention and treatment,” said Dr. Michael Frieser.

A key highlight of the program was a presentation by Prof. Antje Körner, Head of Childhood Obesity and Metabolic Research at HI-MAG. She shared recent findings on metabolic complications in children with obesity and emphasized the importance of early intervention.

“We need to consider and address the origins of diseases such as obesity already in childhood. Understanding metabolic changes in childhood is essential if we want to reduce the burden of obesity-related diseases later in life,” said Prof. Körner.

Further presentations showcased HI-MAG’s vascular research and ongoing clinical studies investigating preventive approaches that could reduce the risk of metabolic diseases in children and adolescents. The presentations also highlighted the importance of longitudinal cohorts.

“Addressing complex questions in obesity and metabolic research requires access to well-characterized cohorts across the entire lifespan such as LIFE Child,” said Dr. Babett Gläser. “Long-term cohort studies provide an invaluable foundation for understanding disease development and identifying risk factors at an early stage.” The delegation also toured through the Clinical Trial Unit to learn more about the different clinical projects and visited HI-MAG’s metabolic chambers, a unique research facility that allows scientists to precisely study energy metabolism in both adults and children.

“The research presented at HI-MAG demonstrates how scientific excellence can contribute to addressing one of the most significant public health challenges of our time. What impressed me most is the institute’s long-term perspective: understanding disease mechanisms early, identifying individuals at risk, and developing concepts that enable prevention before illness occurs.” – Dr. Ulrike Poller

Prof. Matthias Blüher emphasized: “Our vision should be to prevent disease rather than treat its consequences. By identifying risk factors early and intervening at the right time, we have the opportunity to improve long-term health outcomes for future generations.”

The visit highlighted the importance of close exchange between science and policymakers to translate scientific discoveries into effective prevention strategies. Research at HI-MAG can help to pave the way toward a future in which prevention begins earlier, is more targeted, and ultimately more effective.

Rare Diseases as a Gateway to Precision Medicine

VEO-IBD develops during infancy or early childhood and is often characterized by a particularly severe clinical course. In a subset of affected children, rare inherited genetic defects disrupt key pathways regulating programmed cell death, leading to uncontrolled intestinal inflammation.

The funded project uses these rare monogenic disorders as precision models to uncover fundamental molecular mechanisms driving chronic intestinal inflammation. The research focuses on understanding how dysregulated cell death pathways in immune and intestinal epithelial cells initiate and sustain chronic inflammation, and on identifying molecular signaling pathways that may serve as targets for innovative therapeutic interventions.

“Our goal is to translate these discoveries into novel diagnostic and therapeutic strategies, initially for affected children, but ultimately also for patients with more common forms of inflammatory bowel disease,” says Daniel Kotlarz.

From Fundamental Discovery to Clinical Translation

Clinical observations from affected children provide the starting point for experimental investigations, while insights gained in the laboratory are translated into improved diagnostic and therapeutic approaches. The research team combines state-of-the-art multi-omics technologies and computational analyses with innovative human disease models based on induced pluripotent stem cells, including intestinal organoids and immune cells. The long-term objective is to identify and functionally validate novel therapeutic targets in preclinical models for children with severe IBD.

Impact Beyond Rare Diseases

The expected findings extend beyond rare monogenic disorders. Many of the inflammatory pathways investigated in this project are also implicated in more common forms of IBD. Consequently, the project is expected to provide important new insights into the mechanisms of chronic inflammation while opening new avenues for the development of precision therapies with broad clinical relevance. “This award highlights the scientific excellence of pediatric research at Dr. von Hauner Children’s Hospital at the LMU University Hospital Munich. The project combines innovative basic science with a strong translational perspective and has the potential to significantly improve the treatment of children with rare inflammatory diseases,” says Professor Christoph Klein, Director of the Department of Pediatrics at Dr. von Hauner Children’s Hospital, LMU University Hospital Munich.

Strengthening Precision Medicine

This award further strengthens Professor Daniel Kotlarz’s internationally recognized research on rare immunological and inflammatory disorders. Recently, he was awarded a prestigious Heisenberg Professorship by the German Research Foundation (DFG) and appointed Professor of Precision Medicine for Pediatric Inflammatory Bowel Disease in the Department of Pediatric Gastroenterology, Hepatology and Nutrition at the LMU University Hospital Munich. In his dual role as Professor at LMU University Hospital and Group Leader at Helmholtz Munich, Daniel Kotlarz bridges clinical medicine with cutting-edge genomics, computational biology, and translational systems medicine. The Rise up! award further reinforces the close scientific partnership between LMU University Hospital and Helmholtz Munich and provides an outstanding platform to accelerate the translation of fundamental biological discoveries into innovative diagnostic and therapeutic strategies for children with IBD.

“It is a tremendous honour to receive the FEBS | EMBO Women in Science Award”, said Eleftheria Zeggini, Director of the Institute of Translational Genomics at Helmholtz Munich, in Germany. “It serves as an inspiration to pursue bold ideas and help shape the future of science.”

“Scientific excellence is ultimately about changing what we know and what becomes possible. Eleftheria Zeggini has done precisely that through research that has transformed the scale and scope of human genomics and brought genetic discovery closer to understanding and treating disease,” noted Miguel A. De la Rosa, Secretary General of FEBS. “Recognising women who are making contributions of this calibre is at the heart of this award, and FEBS is proud to celebrate Eleftheria as one of the scientists leading her field.”

“I warmly congratulate Eleftheria Zeggini on receiving the 2027 FEBS | EMBO Women in Science Award,” commented EMBO Director Fiona Watt. “Eleftheria embodies the values that EMBO is proud to champion. Her leadership in translational genomics shows what is possible when talented researchers are given the environment to pursue bold, high-quality science throughout their careers, and her contribution to shaping science policy reflects the kind of engagement we hope to see across our community. She is a truly inspiring role model for the next generation of scientists.”

Zeggini is internationally recognized for pioneering work in the genomics of complex human diseases, particularly type 2 diabetes, obesity and osteoarthritis. Her research has helped move the field from large-scale genetic discovery towards a deeper understanding of disease mechanisms and potential clinical applications, integrating population-scale genomics with multi-omics, advanced computational approaches and artificial intelligence. Through the Type 2 Diabetes Global Genetics Initiative, she has led efforts to integrate and analyse genetic data from more than four million individuals worldwide, while improving the diversity and transferability of genetic findings. In osteoarthritis, her work has expanded the number of robustly associated disease loci to more than 930 and helped identify potential therapeutic targets, including opportunities for drug repurposing.

Alongside her scientific achievements, Zeggini has made significant contributions to scientific leadership, mentoring, equality and inclusion. She founded the Institute of Translational Genomics at Helmholtz Munich and has led major interdisciplinary research programmes bringing together genomics, imaging, artificial intelligence and machine learning. She has supported scientists at all career stages and has been a longstanding advocate for greater equality and inclusion in research, including founding the Wellcome Genome Campus Equality in Science programme and organising the first Munich for Women in Science event. Her leadership also extends to science policy, governance and public engagement, where she has contributed to international discussions on responsible data sharing, research sustainability and the future of biomedical science.

“Eleftheria’s leadership is exceptional in its reach, far beyond her own outstanding research. By striving to build scientific environments in which others can grow and thrive, she reminds us of the responsibility we, as scientists, have towards the people and communities both near and far,” commented Anne Ephrussi, Chair of the FEBS Women in Science Working Group. “I hope that seeing women like Eleftheria recognized and visible in science will inspire and help other young researchers to be bold and creative, and to find their own individual ways to shape science.”

The award will be presented at the 51th FEBS Congress in Riga, Latvia, taking place from 3 to 7 July 2027. Zeggini will deliver a plenary award lecture and participate in a lunch event with junior scientists attending the Congress. She will also receive a bronze statuette, a commemorative certificate, and a prize of 10,000 euros.

The FEBS | EMBO Women in Science Award is a joint initiative that recognizes and celebrates outstanding female scientists working in Europe. It highlights both research excellence over the past five years and a commitment to supporting women in science through leadership, mentorship and public outreach.

"One challenge is that cryo-ET images can contain gaps in information due to technical limitations of the imaging process. As a result, certain membrane orientations are difficult or partly impossible to see. This is exactly where MemBrain v2 comes in, automating the process," explains first author Lorenz Lamm.

Optimizing a Key Technology in Cell Biology

MemBrain-seg detects membranes directly, without requiring users to provide additional annotations or training data. MemBrain-pick also requires only a small amount of training data: In one test, researchers manually annotated the positions of protein complexes on just a single membrane. Based on these annotations, the tool localized the corresponding protein complexes on additional membranes with an F1 score of 91 percent. Until now, this 3D image data had to be labeled painstakingly by hand, and the results could rarely be reused for new datasets. Existing programs usually handled only single parts of the analysis – for example outlining the membranes or locating the proteins within them.

Three Tools in One Software – and Little Data Suffices

For the first time, MemBrain v2 combines three steps in a single AI tool: it finds membranes (MemBrain-seg), locates the proteins embedded in them (MemBrain-pick) and measures how these proteins are arranged (MemBrain-stats). 
In several applications, the tool matched the results of painstaking manual analyses, but was considerably faster. It is also easy to use and can be applied to other research questions without major adjustments. Because all components are open source, the membrane-detection module is already widely used around the world and has, for example, been applied across datasets from the Chan Zuckerberg Imaging Institute.

“By making these analyses faster and accessible to research groups worldwide, we can study cellular processes across much larger datasets. This can ultimately help us better understand how cells function – and what changes when disease develops,” says senior author Dr. Tingying Peng.

Larger Datasets and Finer Distinctions Ahead

MemBrain v2 has already contributed to new biological insights: In a separate study, the tool showed that important photosynthesis proteins are spatially separated within the membrane – challenging previous models of their organization. In the future, it is set to distinguish different protein types even more precisely. 

“I’m especially pleased that MemBrain v2 is now being used in many further studies, where it simplifies demanding analyses or makes them possible in the first place – making a concrete contribution to new biological insights,” says first author Lorenz Lamm.

Original Publication

Lamm et al., 2026: MemBrain v2: an end-to-end tool for the analysis of membranes in cryo-electron tomography. Nature Methods. DOI: 10.1038/s41592-026-03178-8

Software: https://github.com/CellArchLab/MemBrain-v2 

Like dancers, proteins are constantly moving, shifting and reshaping. These molecular motions are central to protein function. However, measuring them experimentally remains time-consuming and expensive.

Reid Alderson leads his own laboratory at the Institute of Structural Biology (STB) and Institute of Computational Biology (ICB), respectively part of the Molecular Targets and Therapeutics Center and Computational Health Center at Helmholtz Munich. Through Protein-DANCE, he aims to develop a fast, multiplexed platform based on nuclear magnetic resonance spectroscopy (NMR). The platform will enable protein motions to be measured at high throughput and thus on a much larger scale than is currently possible.

How Molecular Motions Regulate Enzyme Function

Using the new platform, Alderson will investigate diverse families of enzymes, including enzymes designed using artificial intelligence. The aim is to determine how molecular motions regulate catalysis – the process by which enzymes accelerate chemical reactions.

Protein-DANCE will make it possible to measure protein motions on a much larger scale. In this way, the project could help advance structural biology from largely static snapshots towards a dynamic and predictive understanding of molecular mechanisms.

About the ERC

The ERC was established by the European Union in 2007 and funds excellent frontier research across Europe. It supports researchers of all nationalities and at different career stages through several funding schemes, including Starting Grants, Consolidator Grants, Advanced Grants and Synergy Grants. The ERC forms part of Horizon Europe, the EU’s framework program for research and innovation.

In the latest Starting Grant funding round, the ERC is awarding a total of €705 million to 421 researchers across Europe. The grants support researchers at the beginning of their scientific independence, enabling them to pursue ambitious projects and establish their own research teams. Each Starting Grant provides up to €1.5 million over a maximum period of five years. A total of 4,807 proposals were submitted in the latest funding round, of which 8.8% were selected for funding.

MIDAS: Modelling Human Behaviour at Scale

How does the human brain process information and translate it into behavior? Marcel Binz, Postdoctoral Researcher at the Institute for Human-Centered AI at Helmholtz Munich, addresses this fundamental question in cognitive science through his project “Modeling the Integrated minD At Scale” (MIDAS). On 1 October 2026, Binz will join the Max Planck Institute for Biological Cybernetics in Tübingen as a Group Leader.

From Individual Tasks to Integrated Models

Computational cognitive models translate psychological theories into algorithms. In doing so, they can help researchers investigate cognitive processes that cannot be directly inferred from observable behaviour alone. To date, however, such models have generally been tailored to individual tasks or specific research domains. This makes it difficult to integrate findings from different experiments and generalize them to new situations.

MIDAS therefore aims to develop large-scale, integrated models of human cognition. These models will be designed to simulate and predict human behaviour across a range of experimental tasks while also providing interpretable explanations of the underlying cognitive processes. To achieve this, Binz combines approaches from cognitive science, machine learning and language modelling.

A key foundation of the project is Psych-101, a dataset that brings together more than ten million human decisions from 160 experiments in a standardized format. Building on this resource, Binz aims to investigate which cognitive processes operate across different tasks, which are specific to particular situations, and how they interact to generate human behavior.

Cognitive Models for More Naturalistic Settings

MIDAS will also gradually extend cognitive modelling beyond controlled experiments to more naturalistic settings. The planned research includes studies of human conversations as well as complex visual and computer-based tasks. In the long term, the findings could provide a foundation for future applications in fields such as education and psychiatry.

About the European Research Council

The European Research Council was established by the European Union in 2007 and funds excellent frontier research across Europe. It supports creative researchers of all nationalities and at different career stages. Its core funding schemes include Starting Grants, Consolidator Grants, Advanced Grants and Synergy Grants. The ERC forms part of Horizon Europe, the EU’s framework programme for research and innovation.

Research teams at the Institute of Stem Cell Research (ISF) and the Institute of Developmental Genetics (IDG) at Helmholtz Munich and TUM have now constructed an RNA transporter from the ground up. The researchers combined functional protein building blocks with a structural protein designed using generative AI. This protein forms the scaffold of the vehicle and can adopt shapes that do not occur in nature. 

“We did not want to recreate nature, but to design new structures for a specific task: the efficient delivery of RNA,” says Dr. Christoph Gruber, team leader at the ISF and co-first author of the study.

The team tested more than one hundred variants. Surprisingly, protein structures with non-natural geometries performed particularly well. STV-C8 was the most efficient. 

“The fact that a structure that differs so markedly from natural viral capsids works particularly well was a key finding for us,” says Dr. Maren Kirstin Schuhmacher, postdoctoral researcher at the ISF and also co-first author. “It demonstrates the potential of using AI to systematically expand the protein design space.”

In cell culture, STV-C8 delivered RNA into target cells far more efficiently than the virus-like particles and lipid nanoparticles tested. Compared with the lipid nanoparticles, its transfection rate was substantially higher; to achieve comparable protein production, STV-C8 required substantially less RNA. The system could also be loaded with different RNA cargoes and directed toward specific target cells. 

“This modularity is particularly important to us because it allows us to adapt the transporter to different applications and target cells,” says Dr. Florian Giesert, group leader, Gene Editing, at the ISF.

The team tested whether the approach also works in a living organism using animal models. Following intravenous administration in mice, STV-C8 led to expression of the delivered RNA primarily in the lungs; the researchers found no evidence of immunological or toxic side effects. They also loaded STV-C8 with components of the CRISPR/Cas9 system and injected the transporter into the muscle of a pig. There, they succeeded in removing a disease-relevant section of the dystrophin gene. This gene contains the blueprint for a protein that stabilizes muscle cells and is disrupted in Duchenne muscular dystrophy.

STV-C8 is still an experimental system. Before it can be used medically, the researchers will need to investigate, among other things, how the vehicles can be directed specifically to particular cell types and how they distribute throughout the body. 

“With STV-C8, we have created a platform that we can now further develop for a range of therapeutic applications,” says Prof. Wolfgang Wurst, Emeritus of Excellence at Helmholtz Munich and TUM and last author of the publication. The team also plans to transfer the technology into a spin-off company.

Original Publication

Schuhmacher et al., 2026: Creating bottom-up RNA transfer vehicles from synthetic protein assemblies. Nature. DOI: 10.1038/s41586-026-10952-3

Elevated ADAMTSL4 Levels in Cachectic Patients with Colorectal and Lung Cancer

“We wanted to better understand which signals from the tumor trigger the breakdown of muscle and fat tissue,” says Dr. Mauricio Berriel Diaz, last author of the study and research group leader at the Institute for Diabetes and Cancer (IDC) at Helmholtz Munich. 

The team focused on ADAMTSL4, a protein released by tumor cells. In several mouse models of cancer cachexia, the researchers found elevated ADAMTSL4 levels in the blood. Higher ADAMTSL4 levels were also associated with greater weight loss and more pronounced cachexia in patients with colorectal and lung cancer.

To test whether ADAMTSL4 is indeed involved in the development of cachexia, the team specifically altered the amount of the protein in mouse tumor cells. When they switched off ADAMTSL4 production in tumor cells that normally induce cachexia, the animals lost significantly less muscle and fat mass. Conversely, when the researchers increased ADAMTSL4 production in tumor cells that otherwise do not cause cachexia, these cells formed cachexia-inducing tumors. 

“This allowed us to show that ADAMTSL4 is not merely associated with cachexia, but can actively drive the process,” says Dr. Juliano Machado, first author of the study and postdoc at the IDC.

ADAMTSL4 Locally Activates the TGF-β Signaling Pathway

In the next step, the team investigated how ADAMTSL4 exerts this effect. They found that the protein does not directly activate the breakdown of muscle and fat tissue, but rather acts through a known signaling pathway. On the surface of muscle cells, TGF-β1 – an important messenger for cell and tissue remodeling – is initially present in an inactive form. DAMTSL4 binds to a component of this dormant complex and thereby releases active TGF-β1. This then activates signaling pathways that promote protein breakdown in muscle cells and enhance fat breakdown in adipocytes.

This mechanism is particularly interesting for the development of potential therapies because directly blocking TGF-β is therapeutically challenging. The signaling pathway fulfills many important functions in the body; systemic inhibition could therefore be associated with considerable side effects. ADAMTSL4 may offer a way out of this dilemma: The protein is secreted by tumors, is elevated in cachexia, and appears to activate TGF-β locally in the affected tissues. 

“Instead of systemically blocking TGF-β itself, we could in the future try to specifically inhibit an upstream tumor factor – ADAMTSL4,” says Prof. Stephan Herzig, Director of the IDC. “This makes ADAMTSL4 a promising target for the development of new anti-cachectic therapies.”

Further Investigation of ADAMTSL4 as a Potential Therapeutic Target

At the same time, Berriel Diaz emphasizes that cancer cachexia is not a uniform process: “ADAMTSL4 levels are unlikely to be equally elevated in all patients; appetite regulation, inflammatory processes, and other tumor factors may also play a role.”

 The findings therefore also point toward personalized therapeutic strategies: In the future, it may be possible to identify patients with elevated ADAMTSL4 levels for whom targeted blockade of this signaling pathway could be particularly useful. 

“The results provide a basis for further investigating ADAMTSL4 as a therapeutic target,” Berriel Diaz concludes. “Looking ahead, it will be important to determine whether targeted inhibition of this factor can slow the loss of muscle and fat tissue in cancer cachexia.”

"M1 Cachexia Center" to Unite Munich's Cancer Cachexia Research

With the "M1 Munich Medicine Alliance", a new consortium is being established to bring together top-tier biomedical research in Munich. In its inaugural "Innovations for Patients" funding round, researchers at Helmholtz Munich – together with clinical partners at the Technical University of Munich (TUM) and Ludwig Maximilian University Munich (LMU) – secured substantial funding to establish the "M1 Cachexia Center". The center provides an important framework for developing new therapeutic approaches to cancer cachexia, an endeavor to which the present study will contribute.

Original Publication

Machado et al., 2026: Tumor-secreted ADAMTSL4 activates latent TGF-β1 to drive cancer cachexia. Cancer Discovery. DOI: 10.1158/2159-8290.CD-26-0045

The award recognizes the discovery of the fin-loop in glutathione peroxidase 4 (GPX4), a short protein segment that anchors the enzyme in a nerve cell membrane and helps eliminate lipid peroxides that could damage it. Marcus Conrad likened GPX4 to a surfboard: with the fin in the water, it glides along the membrane's inner surface, detoxifying as it moves. Children inheriting the R152H mutation in GPX4 have a board that can no longer catch the wave. Although the enzyme remains present and retains its catalytic ability in laboratory tests, it becomes ineffective when it matters most.

This key structural insight clarified a decade of confusion. It reveals why an enzyme appearing normal in activity assays can cause severe disease, especially affecting neurons with polyunsaturated fatty acid-rich membranes. Additionally, it underscores why ferroptosis, once considered merely a lab curiosity, is now recognized as a significant factor in human neurodegeneration. The research was published in Cell in 2026 and took nearly fourteen years, according to Marcus Conrad.

For the SSMD community, the consequences were immediate and practical. A mechanism now exists to describe: a mutation-specific stem cell and organoid system that mimics the disease, a mouse with the same variant, and a way to test candidate drugs.

Research in Partnership with Affected Families

The Raghav Prize was created for work that could not have happened without patients and families. The three American children whose shared R152H variant started the investigation were found through a family-built network. Skin cells from an affected child were reprogrammed into stem cells and grown into cortical neurons and brain organoids. Parents raised money, kept a registry, chased the sequencing data, and enabled a biobank. CureGPX4's founder, Sanath, is a co-author on the paper, which is where a patient organization belongs when it has done that much of the work.

“When Raghav was diagnosed, we were told there was nothing to work with. No mechanism, no model, no drug, no trial, and a prognosis delivered in a tone that suggested we should stop asking,” said Sanath Kumar Ramesh, founder of the CureGPX4 Foundation. “Marcus and his team spent fourteen years turning that nothing into a structure you can point at on a screen. Plenty of scientists have been kind to my family. Marcus was kind, took our calls, sent us the cells back, and then went and solved it.”

“We named the prize after our son because we want the field to remember who the work is for,” Ramesh added. “Raghav is not a case report. He is the reason this Science exists.”

About the Raghav Prize

The Raghav Prize will be awarded annually to a researcher whose work has materially changed the outlook for an ultra-rare disease and who did that work in partnership with the affected community.

Laureates are asked to do one thing beyond accepting: spend a day with the families of the disease community, in person or online, answering whatever they want to ask, at whatever level of detail they want it. Marcus Conrad has agreed and has proposed that his co-first authors come too.

“Prizes in this business usually come from committees of people who look like me,” said Marcus Conrad. “This one comes from the families who sent us their children's cells and then waited for many years without ever asking us to hurry. It is the one I will keep on the desk rather than the shelf.”

About Sedaghatian-Type Spondylometaphyseal Dysplasia

Sedaghatian-type spondylometaphyseal dysplasia (SSMD) is an ultra-rare autosomal recessive disorder caused by mutations in GPX4. Most affected infants die within days of birth from respiratory failure. The small number who survive live with profound developmental delay, feeding and hearing difficulties, skeletal abnormalities, seizures, and progressive neurodegeneration. Fewer than a dozen children are known to be living with the condition worldwide.
 

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Dezember 2026
Reason for procurement/Produkt:    Mängelbeseitigung BMA G3525
Client/Firma:                                    Siemens AG

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Dezember 2026
Reason for procurement/Produkt:    Mängelbeseitigung BMA G3534 
Client/Firma:                                    Siemens AG

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Dezember 2026
Reason for procurement/Produkt:    Geb.3511 (C+E)  Erweiterung BMA  
Client/Firma:                                    Siemens AG

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Juli 2026
Reason for procurement/Produkt:    div. NovaSeq X Series 10B Reagent Kits  
Client/Firma:                                    Illumina

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Dezember 2026
Reason for procurement/Produkt:    Customized PepMix  
Client/Firma:                                    JPT PEPITIDE TECHNOLOGIES

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Dezember 2026
Reason for procurement/Produkt:    Filterpapierkarten Layout Milano 
Client/Firma:                                    Ahlstrom-Munksjö Group

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Juli 2026
Reason for procurement/Produkt:    div. NovaSeq X Series 10B Reagent Kits  
Client/Firma:                                    Illumina

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Juli 2026
Reason for procurement/Produkt:    Xenium Prime 5K Human Pan Tissue  
Client/Firma:                                    10x Genomics, Inc

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   Juni 2026
Reason for procurement/Produkt:    div. Olink 96.96 IFC for Protein  Kits 
Client/Firma:                                    Olink Proteomics AB

Verhandlungsverfahren ohne TW / Negotiated procedure without prior publication

Threshold/Verhandlungsverfahren:   UVgO
Running time/Zeitraum:                   08/2026-12/2026
Reason for procurement/Produkt:    Change Requests eCRF  
Client/Firma:                                    Qubicon AG

The digital platform is now available at gesund-mit-ki.de (German only). It presents concrete, everyday scenarios across five stages of life. How might intelligent wearables support Clara, 34, and her unborn child throughout pregnancy in 2036? How could AI help diagnose the rare condition of 16-year-old Lena? How might it save the life of Sebastian, 55, after a stroke? And how will assistive robots support older people in need of care ten years from now?

Each story is based on the expertise of researchers at the Technical University of Munich (TUM), Ludwig Maximilian University (LMU), and Helmholtz Munich, and reflects the current state of research. In addition to these patient stories, the researchers also address broader questions such as: “Will people with serious illnesses increasingly be filtered out before birth?” and “How will drugs be developed in the years ahead?”.

Content Developed Through Dialogue

A distinctive feature of the platform is that many of the topics were developed in advance in workshops with members of the public. The aim is to help a broad audience better understand the potential, limitations, and societal implications of AI applications. The project has already been presented at the “Festival of the Future,” and additional public events are planned.

The M1 partners – TUM, LMU and their university hospitals, as well as Helmholtz Munich – are collaborating on the project with Wort & Bild Verlag (including apotheken-umschau.de).

Further Information and Links

M1 – Munich Medicine Alliance was established to promote cutting-edge medical research and the translation of scientific findings into patient care. Its members include the Technical University of Munich (TUM), Ludwig Maximilian University of Munich (LMU) and its university hospitals, as well as Helmholtz Munich.

Science Year 2026 – Medicine of the Future

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Now, an international team led by Prof. Markus Ege from the Institute of Asthma and Allergy Prevention at Helmholtz Munich and the Dr. von Hauner Children’s Hospital at LMU University Hospital has answered this question. The researchers have shown for the first time which specific bacteria in barn air trigger the farm effect, which substances within those bacteria mediate the protection, and which receptors in the body they bind to. Their findings have been published in The New England Journal of Medicine – Evidence.

For years we have been hearing about the hygiene hypothesis, which was first proposed in 1989. This came after three decades of dramatic increases in allergies, asthma, and hay fever among children in Western industrialized countries. These are all conditions in which the immune system mounts an exaggerated inflammatory response and mistakenly attacks the body’s own tissues. According to the hygiene hypothesis, this happens because of under-stimulation in early childhood. The immune systems of children who encounter too few environmental microbes and common cold viruses are more likely to malfunction. “Girls and boys who grow up on farms and are exposed to a wider variety of microbes have the problem far less often,” says Ege. As their immune systems constantly contend with bacterial ‘sparring partners’ from barn air, they are trained to avoid excessive inflammatory responses.

However, the hygiene hypothesis has not been definitively proven, as it is largely based on observational studies. “This kind of research can only show more or less convincing correlations,” says epidemiologist Ege. “But with our new study, we can make a much stronger case, because we can identify the individual links in the proposed causal chain: the bacteria, the relevant microbial metabolic products, and the human receptors.”

The Approach

The researchers analyzed data from more than 1,000 children participating in European studies in rural areas. For all the children, girls and boys, two types of samples had been collected: nasal swabs and mattress dust. In addition, dust samples were taken from cowsheds for 47 farm children. The team examined which bacteria and fungi were present in these samples, how the different microorganisms were related, and whether specific microbial groups protected the children against asthma.

To this end, the epidemiologists and bioinformaticians employed state-of-the-art genetic and metabolic analyses and developed computer models. Through a process of elimination, they eventually identified the key microorganisms. They also investigated whether the children’s own genes influenced this protective effect. To validate their findings, the researchers additionally used data from France and Finland.

The Results

We identified a small number of bacteria, which we can now pinpoint down to the species level,” explains Giulia Pagani, first author of the study and bioinformatician at the Institute of Asthma and Allergy Prevention at Helmholtz Munich, “such as Romboutsia timonensis and Glutamicibacter arilaitensis. These gram-positive bacteria together mediate two-thirds of the entire farm effect for asthma protection and half of the effect for hay fever and atopic eczema.” The bacteria originate in the cow’s digestive tract, where they produce or metabolize substances like kynurenine, xanthine, alpha-linolenic acid, and stearidonic acid. These compounds are easily inhaled and recognized by two receptors on human airway cells – AhR and PPARγ. “These receptors,” Ege continues, “have multiple functions, including in the immune system, where they appear to prevent excessive inflammatory responses.” Their role in the farm effect was previously unknown. For the first time, therefore, the complete biological chain is visible: cow → barn air → bacteria → metabolic products → human receptors → protection against asthma.

The new findings can now be used by laboratory researchers to decipher the molecular and cellular mechanisms of the farm effect. This opens up the prospect of developing a drug that mimics the farm effect – without the need for children to spend time in barns.

Original Publication

Pagani et al., 2026: Gram-Positive Bacteria and the Inverse Association between Farm Exposure and Childhood Asthma. NEJM Evidence. DOI: https://doi.org/10.1056/EVIDoa2500271