The Else Kröner-Fresenius-Stiftung (EKFS) will confer the Publication Prize 2025 to five outstanding scientists during the second Alumni Day taking place today in Frankfurt am Main. The prizewinners are being recognized for their particularly excellent findings, which they published in 2024 and achieved thanks to funding from the EKFS. Each of the prizes is endowed with €10,000 that the prizewinners are free to spend at their own discretion.
The EKFS’s Scientific Commission has selected the following scientists for recognition:
Prof. Dr. Ricardo Grieshaber-Bouyer, Department of Internal Medicine 3 – Rheumatology and Immunology, Friedrich-Alexander University (FAU) Erlangen-Nuremberg and Erlangen University Hospital, for his paper “Bispecific T cell engager therapy for refractory rheumatoid arthritis” published in Nature Medicine: https://www.nature.com/articles/s41591-024-02964-1
Rheumatoid arthritis is a chronic autoimmune disease that causes joint inflammation. Various immunosuppressive drugs have been approved for its treatment, however a significant proportion of patients do not respond well to the established treatments. B cells play a crucial role in rheumatoid arthritis. During the study, Ricardo Grieshaber-Bouyer and his team used T cell engagers for the first time to treat rheumatoid arthritis. T cell engagers act as a bridge between T cells and B cells, leading to the elimination of the B cells. The treatment using the T cell engager blinatumomab was well tolerated, effectively reduced the B cells in the blood and joints, and significantly reduced joint inflammation. T cell engagers could therefore present a new treatment option for patients with rheumatoid arthritis and other autoimmune diseases.
Dr. Jan-Michel Heger, Department I of Internal Medicine, University Hospital Cologne, for his paper “Circulating tumor DNA sequencing for biologic classification and individualized risk stratification in patients with Hodgkin lymphoma” published in the Journal of Clinical Oncology: https://doi.org/10.1200/JCO.23.01867
In this prizewinning project, Jan-Michel Heger and his team explored the genetic fingerprint of Hodgkin lymphoma extensively. Hodgkin lymphoma is a malignant tumor that mainly affects young adults. While most patients can be cured with chemotherapy and radiotherapy, they subsequently have to live for decades with possible long-term damage, such as infertility or the impaired functioning of vital organs. With the help of a single blood sample, the researchers were able to examine the genetic fingerprint of Hodgkin lymphoma in small snippets of DNA from the tumor tissue of several hundred patients. They identified three different subtypes of Hodgkin lymphoma, two of which show changes that suggest a very good efficacy of immunotherapies. To reduce the side effects and long-term damage caused by chemotherapy and radiotherapy, the aim is to now use targeted immunotherapy to treat patients with Hodgkin lymphoma whose tumor has a corresponding genetic fingerprint.
Felicitas E. Hengel, III. Department of Medicine (Nephrology/Rheumatology/Endocrinology), University Medical Center Hamburg-Eppendorf, for her paper “Autoantibodies targeting nephrin in podocytopathies” published in The New England Journal of Medicine: https://www.nejm.org/doi/pdf/10.1056/NEJMoa2314471
Autoimmune diseases of the kidney (including “minimal change disease”, “primary focal segmental glomerulosclerosis,” and “idiopathic nephrotic syndrome”) lead to significant protein loss in patients’ urine. The resulting protein deficiency gives rise to lipometabolic disorders, immune deficiency, and fluid retention in the body. In order to understand the cause of these diseases, Felicitas E. Hengel and her team investigated the occurrence of autoantibodies against nephrin in patients – a signaling protein of the cells in the kidney that form the kidney’s blood-urine barrier. They developed a new test procedure for the reliable quantification of anti-nephrin autoantibodies and were able to detect them in the blood of the majority of patients. The antibody titers correlated with the disease activity. They also developed an animal model in which they were able to investigate the pathomechanisms of anti-nephrin autoantibodies. The study enables a new understanding of the cause of the disease and paves the way for more precise diagnostics, a more accurate prognosis, and causal therapy.
Dr. Susanne Meinert, Institute for Translational Psychiatry, University of Münster, for her paper “Associations between white matter microstructure and cognitive decline in major depressive disorder versus controls in Germany: a prospective case-control cohort study” published in Lancet Psychiatry : https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(24)00291-8/fulltext
Cognitive deficits such as concentration and memory problems not only affect people with depression in acute phases of their illness, but often beyond this. The most comprehensive longitudinal study on this topic to date with 881 participants (418 of whom had depression) has now revealed that those affected suffer from severe cognitive deficits. At the same time, the integrity of central brain fiber connections deteriorates more rapidly over time. These changes as well as an unfavorable course of the disease (e.g., more phases of illness during the study period) independently predicted further deterioration of the cognitive capabilities. The findings, which proved to be extremely robust despite numerous statistical corrections, emphasize that changes in the brain structure and the prevention of new depressive episodes are decisive focal points for future treatment strategies.
Marcel S. Woo, Institute of Neuroimmunology and Multiple Sclerosis, University Medical Centre Hamburg-Eppendorf, for his paper “STING orchestrates the neuronal inflammatory stress response in multiple sclerosis” published in Cell: https://linkinghub.elsevier.com/retrieve/pii/S0092867424005762
Multiple sclerosis (MS) is a chronic inflammatory disease of the brain and spinal cord. The persistent inflammation destroys nerve cells and leads to neurological deficits. Current treatments cannot stop or slow this process. In the study, Marcel S. Woo and his team were able to identify a new signaling pathway that contributes to neurodegeneration. They discovered through a combination of bioinformatic, biochemical, and genetic analyses that the “STING” protein is only upregulated in nerve cells during inflammation and activates a specific cell death signaling pathway. Blocking this signaling pathway protects against neurodegeneration in preclinical MS models and presents a new approach for the treatment of MS and possibly also other neurological diseases.