In the DESYNA project, researchers from the Department of Biomedicine, the Department of Clinical Medicine, and iNANO are collaborating with the biotech company Draupnir Bio to develop a new treatment that specifically degrades aggregates of the protein alpha-synuclein in the brain. These aggregates play a central role in the development of the disease and its spread between neurons.

The new approach combines advanced protein degradation technology with cutting-edge research in neurodegeneration. The goal is to halt disease progression by both removing harmful protein aggregates and preventing their spread.

This project places Denmark at the forefront of Parkinsons disease research and represents an ambitious strategy that offers hope to patients living with the disease, says Associate Professor Simon Glerup from the Department of Biomedicine and CSO at Draupnir Bio, who leads the project.

The project has received a Grand Solutions grant running over three years and aims to deliver new treatment candidates that can be further developed towards clinical testing.

The news is based on press material from Draupnir Bio.

Contact
Associate Professor and Chief Scientific Officer Simon Glerup
Aarhus University, Department of Biomedicine and Draupnir Bio
Phone: +45 51 22 17 27
Email: glerup@draupnir.bio

An examination of this biological trace is now being presented by the British TV station Channel 4 in a two-part documentary: Hitlers DNA: Blueprint of a Dictator.

An international research group, including a team of researchers from the Department of Biomedicine at Aarhus University led by Professor Ditte Demontis, has mapped parts of Hitlers genome based on the bloodstain that an American officer cut out of the sofa upholstery.

The analysis paints the picture of a man with unusual biology but also a picture that requires considerable caution in interpretation.

Debunking the myth of Jewish ancestry

The analysis of Hitlers DNA helps dispel the myth that he supposedly had Jewish ancestry. But it reveals something else: Adolf Hitler stands out genetically when it comes to predisposition for certain psychiatric disorders and brain developmental conditions.

Professor Ditte Demontis and her research group conducted what is known as a polygenic risk score test. This summarizes into a single number the common genetic variants in a persons genome that increase the likelihood of a disorder such as schizophrenia. By comparing the score with that of other people in the population, one can determine where a persons genetic baseline lies relative to others in terms of the risk of developing a given disease or psychiatric condition.

And here, Hitler stands out, the researcher explains:

I was surprised that Adolf Hitler ranks in the top 1 percent for the polygenic score for autism, schizophrenia, and bipolar disorder. None of the 37,000 population-based individuals scored as high on all three parameters. He therefore stands out extremely from the general population, says Ditte Demontis.

Surrounded by mystery and speculation

But the surprising finding does not mean that Hitler necessarily had a psychiatric diagnosis or developmental disorder. Among people in the Danish population with a score equivalent to Hitlers, the likelihood of being diagnosed with autism, bipolar disorder, or schizophrenia is about five percent.

I want to strongly emphasize that the study cannot be used to diagnose the notorious dictator. And polygenic scores do not say anything about a persons morals or actions. Making that link is not scientifically valid, says Ditte Demontis.

The study has value as a scientific and historical exploration. It can contribute to examining myths and generating scientific information within a narrative that for decades has been shrouded in speculation, she says, noting that the hypothesis that Hitler had a psychiatric disorder has existed for many years.

Through his DNA, we now have the opportunity, at a purely genetic level, to shed light on some of the questions that have been raised over time, she says.

A hidden condition: Kallmann syndrome

One of the most striking findings is that, according to the genetic profile, Hitler likely had Kallmann syndrome a rare hormonal disorder that inhibits pubertal development. It can lead to underdeveloped genitalia and fertility problems. For some individuals, it can also make sexual relationships difficult.

The finding provides a biological perspective on longstanding historical speculation about Hitlers sexuality and complex relationships with women.

Professor Ditte Demontis was not responsible for the sequencing of Hitlers DNA, but she was contacted afterward to perform scientific analyses.

The main figure behind the study is British geneticist and biologist Professor Turi King, known for her work in forensic genetics and historical DNA research.

I agreed to illuminate Adolf Hitlers genetic profile regarding predispositions for psychiatric conditions because it was important that it be done scientifically robustly, and that the results be communicated correctly, says Ditte Demontis.

The study expands the understanding of Hitler as a historical figure by also including his biology. It provides a glimpse of how we can apply modern genetic technologies to historical individuals and it raises important questions about how such data should be interpreted responsibly.

Contact

Professor Ditte Demontis
Aarhus University, Department of Biomedicine
Phone: +45 28 53 97 46
Email: ditte@biomed.au.dk

This is an effective but demanding solution with a risk of complications.

Thats why researchers have long been searching for artificial materials that the body can accept and naturally integrate for treating skull injuries.

One of the most promising materials is polycaprolactone (PCL) - a plastic-like substance that slowly dissolves in the body. Until now, it was believed that the immune system hindered its integration.

But in a new study, researchers from the Department of Biomedicine at Aarhus University and the Clinical Institute at Aalborg University suggest a more nuanced view.

The study was recently published in the scientific journal Frontiers in Immunology, and through advanced analyses of PCL implants - including from cranial surgeries in pigs - the researchers discovered that immune cells dont just try to break down the material - they can actually reinforce it.

Immune cells - monocytes and T lymphocytes - are quickly recruited to the implant and form special giant cells that interact with the material and deposit structures that make it more robust, explains clinical lecturer at Aalborg University, Halldór Bjarki Einarsson, the studys lead author.

A dual role for the immune system

The researchers found that it is primarily spontaneous hydrolysis - a chemical process that occurs without cellular help - that breaks down the PCL material. Instead, the immune cells contribute stability. Among other things, they secrete molecules that form strong bonds to the surface of the material.

The result is a surprisingly strengthened implant in the early stages after insertion, says Professor Thomas Vorup-Jensen from the Department of Biomedicine at Aarhus University, who is also involved in the study.

The hypothesis was that cells would degrade the material since its a foreign object. But we discovered that immune cells can be both enemy and ally. They can contribute to inflammation but also to strengthening and integrating the implant, and thats a significant shift in our understanding, he explains.

Implications for future implants

The study opens new doors for both doctors and researchers. By understanding and targeting the immune systems response, they may one day develop implants that cooperate with the body instead of being rejected by it.

This brings hope for better, safer, and more durable solutions for patients with severe bone injuries, says Thomas Vorup-Jensen.

Next, the researchers want to study how these mechanisms operate in humans or animal models over longer periods. The goal is to gain a more precise understanding of how the entire body affects implants - and how best to manage the biological response.

Behind the study

• The study is basic research.
• Collaborating partners from Denmark and abroad: AU Engineering, Vrije University Medical Center, Amsterdam, Netherlands and Stanford University School of Medicine, California, USA.
• The work stems from the so-called LUNA center at Aarhus University - a cross-disciplinary center (The Lundbeck Foundation Nanomedicine Centre for Individualized Management of Tissue Damage and Regeneration), originally led by Dean of Health Allan Flyvbjerg and Prof. Jørgen Kjems (iNANO).
• External funding: The Danish Council for Strategic Research.
• Read more in the scientific article: https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1572238/full

Contact

Professor Thomas Vorup-Jensen
Aarhus University, Department of Biomedicine
Phone: +45 21 48 97 81
Email: vorup-jensen@biomed.au.dk 

Clinical Lecturer and Physician Halldór Bjarki Einarsson
Aalborg University, Clinical Institute and Aalborg University Hospital
Phone: +45 50 40 38 39
Email: halldorbe@dcm.aau.dk 

This text is based on mashine translation

The solution may lie in a small primate from Madagascar. New research shows that stem cells from the small gray mouse lemur are much more closely aligned with human biology than those from the mouse, which is otherwise the most commonly used laboratory animal in labs around the world. And this could be a gamechanger for the development of new treatments.

"We have discovered and isolated adult stem cells in mouse lemurs for the very first time," says Antoine de Morree, Associate Professor at the Department of Biomedicine at Aarhus University, and senior author behind the study.

"We are looking at both muscle stem cells and mesenchymal stem cells - and they behave very differently from mouse stem cells."

Human-like cells in a miniature primate

The study, recently published in the scientific journal Nature Communications, shows that muscle stem cells from mouse lemurs divide more slowly than those from mice and resemble human stem cells more closely.

Researchers also discovered two new mechanisms that may explain some of the differences in stem cell function between humans and mice: Mouse lemur and human muscle stem cells produce less of the compound spermidine, which is crucial for cell function. By adding spermidine, the researchers were able to enhance the cells ability to divide - a discovery now set to be tested in clinical trials at Steno Diabetes Center Aarhus.

Mouse lemur muscles contain fat cells - something seen in humans as well, but not in mice. This is due to the mouse lemurs mesenchymal stem cells being particularly adept at forming fat. These cells produce large amounts of a protein called Complement Factor D, which plays a role in fat accumulation. This is significant because fat in muscle is associated with aging and disease.

"This means the mouse lemur is not only a better model for human muscle - it also offers us entirely new potential treatment targets for diseases and symptoms that do not normally occur in mice," says Antoine de Morree.

Finding the right model organism

The work started when the researchers looked for ways to identify new model organisms. They developed a new computational method to compare cells and tissues between different animals.

In doing so, they found that mouse lemur muscles are very similar to human muscles. Something they could confirm with microscopy.

This new method could greatly reduce animal usage by enabling researchers to identify the optimal animal model before doing any animal experiments. In this case, the researchers were confident to start exploring mouse lemur biology.

It is very exciting to challenge existing paradigms and in the end be able to study something that could not be modeled before, says Pilar Stella, PhD student and the co-first author of the study.

Closer to effective treatments

Although stem cells have long been hailed as the key to regenerative medicine, only a few stem cell therapies are currently approved. A major reason is that many promising results from mouse studies do not translate to humans. With the mouse lemur as a new model, researchers can now develop therapies based on cells that more closely resemble our own.

"This brings us closer to effective treatments for conditions like muscular dystrophy, age-related muscle loss, and other diseases where stem cells could play a role," says Antoine de Morree.

The next step is to test how best to deliver stem cells into muscle tissue in mouse lemurs, and how to fine-tune dosage and treatment timing. Meanwhile, the first human trial using spermidine is being prepared.

About the research results

• The study is basic research
• Collaborator: Stanford University. Other AU researchers involved with the study were PhD student Zofija Frimand, research-year student Anne-Sofie Clausen, Associate Professor Jean Farup and Associate Professor Ermelinda Porpiglia.
• External funding: National Institutes of Health, Novo Nordisk Foundation, Independent Research Fund Denmark (Danmarks Frie Forskningsfond) and Aarhus University Research Foundation
• Read more in the scientific article: https://www.nature.com/articles/s41467-025-58897-x

Contact:

Associate Professor Antoine de Morree
Aarhus University, Department of Biomedicine
Phone: 60 79 07 22
Email: demorree@biomed.au.dk

Researchers from Aarhus University have developed a method that quickly and easily provides doctors with more knowledge about disease progression.

Their study has just been published in Journal of Translational Autoimmunity. The researchers demonstrate a method that shows promise as a biomarker for disease activity in rheumatoid arthritis and, presumably, other autoimmune diseases.

The large proteins are the problem 

The researchers have previously demonstrated the importance of monitoring large proteins in blood samples from patients with Lupus and Alzheimers in order to track disease progression. They have now published an analytical method that shows promise for large-scale clinical application. 

"We have shown that large proteins are a marker for disease activity in both neurodegenerative and autoimmune diseases. The key point is that we have developed an entirely new kind of biomarker that isnt measured today," says Assistant Professor Kristian Juul-Madsen from the Department of Biomedicine at Aarhus University, who is the last author of the study.

Just get started

The new method identifies large immuno-active complexes in patients with inflammation in the study exemplified by rheumatoid arthritis. And this is done in a way that makes it possible to measure patient samples parallelly instead of serially. This will significantly increase capacity. 

"You go from being able to analyse a few samples a day to potentially several hundred. It takes time to implement new assays in the clinical biochemistry departments of hospitals, but this method can be implemented without training new staff or investing in new equipment. You just have to buy the reagents and get started," says Kristian Juul-Madsen.

The study has examined blood and synovial fluid samples from patients with rheumatoid arthritis. The typical patient diagnosed is a woman in her fifties and the disease requires lifelong treatment. But it is important to ensure the medication dosage is neither too high nor too low. A dosage that is too low causes joint deformity, too high causes side effects and the risk of complications.

The new method provides a more precise assessment of disease progression and makes it easier to adapt treatment to the individual patient. 

Also applies to Alzheimer's and Parkinson's

Associate Professor and Rheumatologist Tue Wenzel Kragstrup has served as the study's link to the clinic through his work at the Department of Arthritis and Connective Tissue Diseases at Silkeborg Regional Hospital and Aarhus University Hospital. 

He has collected samples from rheumatoid arthritis patients and developed the assays that will be used to analyse the samples. 

"Better diagnostics lead to better treatment. With the new method, we make it practically possible to improve diagnostics and monitoring in a healthcare system under time pressure," says Tue Wenzel Kragstrup. 

 "The next step is to use exactly the same method on different patient cohorts. Testing other autoimmune conditions would be a logical next step, such as using urine samples for autoimmune kidney diseases or stool samples for autoimmune intestinal diseases," he says.

The results are, of course, particularly exciting for patients and doctors. But the study is also interesting for immunologists trying to understand mechanisms in the immune system, says co-author Professor Thomas Vorup-Jensen.

"Oligomerisation (a process by which small molecules combine to form larger structures) of immuno-relevant proteins is crucial for their activity. Even small concentrations of these large complexes can account for the vast majority of the immune systems response. We have also demonstrated this phenomenon in diseases such as Alzheimer's and Parkinson's, and it is a field in rapid development," he says. 

The research results - more information 

    The study is a combination of translational research, where the researchers develop new biomarker tools for clinical practice, and basic research, where the researchers try to understand the mechanism behind the biomarker that has been found.
    The most important partner is the Rheumatology Research Group, Department of Inflammation and Ageing, University of Birmingham
    External funding: Independent Research Fund Denmark and the Lundbeck Foundation.
    Read more in the scientific article: https://doi.org/10.1016/j.jtauto.2025.100266

Contact

Assistant Professor Kristian Juul-Madsen
Aarhus University, Department of Biomedicine 
Mobile: +45 61 28 55 20 
Email: juul-madsen@biomed.au.dk

Professor Thomas Vorup-Jensen
Aarhus University, Department of Biomedicine 
Mobile: +45 21 48 97 81
Email: vorup-jensen@biomed.au.dk

Associate Professor Tue Wenzel Kragstrup
Aarhus University, Department of Biomedicine, Department of Molecular Medicine (MOMA), Department of Clinical Medicine and Department of Arthritis and Connective Tissue Diseases, Silkeborg Regional Hospital
Mobile: +45 29 82 17 39
Email: kragstrup@biomed.au.dk