DFG Clusters of Excellence, SFB and other DFG projects

Clusters of Excellence with spokespersonship

The Clusters of Excellence (EXC) funding line aims to promote internationally competitive research fields in universities and university alliances on a project basis, including across scientific disciplines. Clusters of Excellence can be funded for seven years per funding period as part of the Excellence Strategy. The LMU Faculty of Medicine is currently the spokesperson for a Cluster of Excellence together with the Technical University of Munich.

EXC 2145: SyNergy - Munich Cluster for Systems Neurology
LMU Speaker: Prof. Dr. Martin Dichgans
Institution: Institute for Stroke and Dementia Research (ISD)
Funding: since 2019

Website
Topics: SyNergy—the Munich Cluster of Systems Neurology—defined Systems Neurology as a new research field where systems-level biology and systems neuroscience meet clinical neurology. Backed by the two Munich Excellence universities and five Helmholtz and Max Planck institutes, this long-term program has yielded remarkable insights and established permanent infrastructure. To date, SyNergy has: revealed numerous new disease-spanning pathomechanisms, including potential leverage points for improved diagnosis and treatment of major degenerative, inflammatory, and vascular CNS diseases, several of which are in transit to clinical exploration; supported >25 Tandem Projects and published >600 papers in high-impact journals, resulting in a leadership role of Munich neuroscience in Alzheimer’s disease, multiple sclerosis, and stroke research; recruited and promoted rising star scientists, allowing us to rejuvenate and diversify the principal investigator team while filling gaps in our research portfolio and increasing measures of excellence (e.g., >25 ERC grants); built two trans-institutional and translational SyNergy Research Centers to integrate the Cluster’s basic and clinical research, readying us for an additional translational push; established Technology Hubs to provide broad access to cutting-edge omics and imaging expertise; expanded support for early career investigators and clinician-scientists, promoted gender equality and diversity and established key research data management infrastructure, in co-operation with our partner institutions. In the next funding period, SyNergy will: boost our capacity to understand, diagnose, and treat major CNS diseases by adding new technologies, expertise, and concepts related to disease-spanning mechanisms; continue funding Tandem Projects to integrate new concepts and researchers while also developing established collaborations into larger Teams dedicated to key Research Topics centered on disease-spanning principles to accelerate target transition; broaden our capabilities to perform Cluster-initiated proof-of-concept studies in humans via new clinical trials units at the SyNergy Research Centers in collaboration with the “M1–Munich Medicine Alliance”, a new initiative by the Bavarian state to extend the trans-institutional integration pioneered by SyNergy to Munich’s entire university medicine; initiate new professorships focused on neuroepigenetics, systems neuroscience, and high-hesolution imaging while also contributing to other relevant recruitments; expand our Technology Hubs to add dedicated support for disease-spanning data integration, AI expertise, and target transition towards the clinic; evolve and grow our support programs by creating a unified M.Sc. and Ph.D. training track, expanding mentoring, integrating medical-scientist, clinician-scientist, and clinician-trialist training, and joining an international postdoc network funded by the NOMIS foundation..

Source: DFG

Podcast episode ‘Alzheimer's - development, findings, research questions of the Cluster of Excellence podcast Exzellent erklärt - Spitzenforschung für alle (published on 4 October 2021)

The podcast on dementia research: clearly explained – podcast series of the SyNergy Cluster of Excellence (10 episodes, published at intervals of approx. 3 weeks from September 2023)

Collaborative Research Centres with spokespersons

Collaborative Research Centres (SFB) are university research institutions funded by the German Research Foundation (DFG) for up to twelve years.

The following list contains all DFG Collaborative Research Centres and Transregios with spokespersons or co-spokespersons from the LMU Faculty of Medicine. In addition, the Faculty of Medicine is involved in numerous SFB sub-projects and as a location in Transregios without a spokesperson function.

SFB 1744: Compartmentalized Cellular Networks in Neurovascular Diseases
Speaker: Prof. Dr. Martin Dichgans
Institution: Institute for Stroke and Dementia Research (ISD)
Funding: since 2026

Website: Project description DFG
Topic: Neurovascular diseases (NVDs) are the leading cause of long-term disability, the second most common cause of death, and a major contributor to dementia worldwide. Despite their high burden, most patients lack specific treatments. Recent research has uncovered a surprising complexity in NVDs, with poorly understood mechanisms that hold promise for novel therapeutic targets. Advances in single-cell omics and imaging have revealed an unexpected cellular diversity and compartmentalization in the brain, which appear to shape disease processes. This includes (1) vascular zonation of endothelial and mural cells; (2) distinct immune interfaces such as the choroid plexus and subsets of adaptive immune cells; and (3) glial cells with compartment-specific states, including in perivascular niches. We hypothesize that NVD progression and complications are driven by compartmentalized cellular networks (CCNs) - functional networks of vascular, immune, and glial cells that support neuronal health, contribute to disease, and offer potential treatment targets. Our aim is to understand how interactions between distinct cell types within anatomical compartments influence disease course and outcome. Our strategy focuses on both chronic and acute NVDs that directly impact brain vasculature, including cerebral small vessel disease (SVD), cerebrovascular amyloidosis, ischemic stroke, and intracerebral/subarachnoid haemorrhage. We will investigate how vascular dysfunction and immune/glial responses impair neuronal function. Building on key discoveries by CRC1744 members in NVD biology, compartmentalization, and cellular responses, we will leverage existing models, tools, and technologies to systematically study these mechanisms. Our methodological approach integrates expertise from neurovascular biology, immunology, glia/stem cell biology, genetics, and data science. We will combine single-cell and spatial transcriptomics with advanced imaging and genetic tools. In addition to experimental animal models, we will conduct mechanistic studies on human iPSC-based models of the neurovascular unit, transplanted human organoids, and in-vivo multicellular recordings in patients. Harmonized models and shared platforms across projects will enable comparative analyses and strengthen collaboration. We will initially focus on ischemic NVDs and expand to haemorrhagic forms in the second funding phase. As a step towards clinical translation, later funding periods will include pre-clinical randomized trials and large animal models. Our long-term goal is to translate findings from model systems to patients and identify compartment-specific therapeutic targets. Achieving this goal requires the structure of a CRC: the complexity of NVD biology, and the technical challenges in dissecting cellular crosstalk across compartments, demand a multidisciplinary, collaborative framework with integrated methods and a joint long-term strategy for data sharing.

Source: DFG

TRR 425: DEFINE - Desmosomal dysfunction in epithelial barriers
Co-Speaker: Prof. Dr. Jens Waschke
Institution: Chair of Vegetative Anatomy, Institute of Anatomy
Funding: since 2026

Website: Project description DFG
Topic: Desmosomes are adhesive cell-cell junctions that provide mechanical resilience and spatially coordinate signalling to control complex epithelial. The skin and the digestive tract are critical barriers between the human body and the environment. There is increasing evidence that desmosome dysfunction leads to loss of epithelial barrier function and is central for the onset and/or perpetuation of inflammatory disorders of human epithelial organs. The focus of the TRR 425 “Desmosomal dysfunction in epithelial barriers” (DEFINE) will be on three human model diseases of desmosomal dysfunction, i.e. pemphigus vulgaris (PV), inflammatory bowel diseases (IBD) and eosinophilic oesophagitis (EOE). PV is caused by autoantibodies against components of desmosomes and presents with severe blistering of skin and mucosal surfaces, major risk of infections and increased body catabolism. IBD and EOE are also characterised by loss of barrier function of the intestinal mucosa and are linked to desmosomal dysfunction in a subset of patients. In this consortium, basic researchers in cell biology and immunology with a focus on desmosomes in epithelial homoeostasis will join forces with clinician scientists dealing with human disorders of skin and digestive tract. This blend of researchers will be able to perform desmosome-related research on a much more complex level based on their shared views and insights. Focusing on proper and impaired desmosomal function of the major epithelial organs will be a novel, most instructive way to understand the complexity of desmosomal functions. We will first study the consequences of desmosomal impairment for disease pathogenesis. This will lead to a thorough understanding of desmosome function in epithelial homoeostasis by the regulation of barrier integrity, cellular signalling, tissue regeneration, and wound healing. Several members of this consortium have a common history in desmosome research based on their participation in FOR 2497 “Pemphigus – from Pathogenesis to Therapeutics” and the SPP 1782 “Epithelial intercellular junctions as dynamic hubs to integrate forces, signals and cell behaviour”. Initially, we will aim at identifying cell type-specific and common pathophysiologic traits in desmosomal dysfunction which induce distinct inflammatory signatures and clinical pathologies in skin and digestive tract. DEFINE will provide mechanistic links between desmosome defects and disease pathogenesis in the digestive tract. These findings will be exploited for targeted therapeutic strategies aimed at restoring desmosomal function. To foster research in this evolving field, we will make major efforts to train a new generation of early career scientists and clinical scientists at the cross-roads between basic and translational science. The TRR 425 DEFINE will close the gap between our limited understanding of fundamental functions of desmosomes in health and the impact of desmosomal dysfunction on human diseases.

Source: DFG

TRR 338: LETSIMMUN - Lymphozyten Engineering für Therapeutische Synthetische Immunität
Co-Speaker: Prof. Dr. Marion Subklewe
Institution: Department of Medicine III
Funding: since 2021

Website: Project description DFG
Topic: The scientists will use various lymphocyte engineering technologies to manipulate lymphocytes with the utmost precision so that they develop specific receptors in an optimised and temporally controllable manner. In addition, various regulators and safety mechanisms will be used to make the synthetic T cells resistant to defence mechanisms and safe to handle. The aim is to establish this immunotherapy as a safe, effective and widely accessible treatment that can be used in various clinical areas, such as cancer therapy, infectious diseases and autoimmune diseases. The spokesperson for the SFB/Transregio is Professor Dirk Busch from the Technical University of Munich (TUM). The spokesperson at the LMU Medical Centre is Professor Tobias Feuchtinger, Head of the Department of Paediatric Haematology, Oncology, Haemostaseology and Stem Cell Transplantation at Dr. von Hauner Children's Hospital. The University of Würzburg is also involved.

Source: LMU Medical Centre

TRR 205: The adrenal gland - central relay in health and disease
Co-Speaker: Prof. Dr. Martin Reincke
Institution: Department of Medicine IV
Funding: since 2017

Website: Project description DFG
Topic: The adrenal gland is the central relay of the human body, coordinating responses to acute and chronic stress factors and integrating endocrine, neuronal, vascular, metabolic and immunological signals. Untreated adrenal insufficiency is fatal, and adrenal hyperfunction caused by adrenal tumours can have life-threatening consequences. Any dysregulation of adrenal function can cause or exacerbate acute and chronic disorders, which is associated with significant morbidity and socioeconomic damage. In our Collaborative Research Centre/Transregio (CRC/TRR) 205, we have not only brought together leading adrenal experts, but also achieved an exceptionally high level of interdisciplinary interaction. This collaborative spirit and the co-operation with leading international experts from other research areas enabled us to make significant progress in many areas of adrenal research during the first funding period. These sustained interactions led to the inclusion of two new projects in the second funding period. Three renowned locations with 18 projects from two research areas and four service projects are participating in this SFB/TRR. Research area A investigates the underlying pathophysiology of adrenal diseases and the role of the adrenal glands as an important relay in systemic disorders, thereby forming the basis for the development of novel therapeutic strategies. Research Area B focuses on the pathogenesis, diagnosis and evaluation of promising new therapies for the most clinically relevant adrenal tumours - phaeochromocytomas/paragangliomas, neuroblastomas, adrenocortical carcinomas, aldosterone- and cortisol-producing adenomas and tumours of the hypothalamic-pituitary axis with their downstream signalling pathways controlling adrenal function. Each project pursues a translational strategy from the laboratory bench to the bedside or vice versa. To best support this, we have established an unparalleled platform of state-of-the-art modelling systems and extensive patient data and materials. Our comprehensive tissue and plasma sample collections and associated clinical cohorts are among the largest of their kind in the world and are essential to make the necessary progress in the field of adrenal diseases.
Source: DFG

SFB 1123: Atherosclerosis - mechanisms and networks of new therapeutic target structures
Speaker: Prof. Dr. Christian Weber
Institution: Institute of Cardiovascular Prevention
Funding: since 2014

Website: Project description DFG
Topics: Arterial vascular diseases, such as coronary heart disease (CHD) and sleep apoplexy, remain the leading cause of death worldwide and impose enormous socioeconomic costs. This dilemma could be alleviated by improved vascular prevention and therapy, which requires a deeper mechanistic understanding of atherosclerosis as an underlying pathology to enable more efficient identification of candidates for potential drug development. In addition to the discovery of PCSK9 inhibitors for better control of hyperlipidaemia, the positive outcome of the CANTOS study has provided clear evidence for the importance of inflammatory signalling pathways in the pathogenesis and therapy of atherosclerosis. Therefore, the mission of the CRC1123 continues to develop a detailed understanding of molecular networks in atherogenesis, atheroprogression and atherothrombosis and thus to advance the identification and validation of relevant therapeutic targets. The identification of therapeutic targets within such networks requires the unbiased testing and selection of candidates on a solid pathogenetic basis and the analysis of their interactions in model systems. In SFB1123 we plan to continue with the systematic elaboration and linking of mechanisms of diverse molecular families (cytokines, signalling proteins, nucleic acids and lipid mediators). State-of-the-art technologies, such as genome editing and conditional mouse models for gene deletion and cell labelling, proteomics, single cell sequencing, spatial transcriptome analysis and bioinformatics, as well as the latest imaging methods (optoacoustics, nanoscopy, MS imaging) will be implemented to track cell movement, function, subcellular and molecular events in plaques or adventitia, to set new standards for the SFB1123 and to close methodological gaps. Based on excellent infrastructure, cooperation culture and recruitment of young scientists, the CRC1123 will further decipher molecular and cellular determinants of atherosclerosis and uncover new links between genetic, inflammatory and metabolic factors. By clarifying interactions and combined effects, the CRC1123 will identify valuable target structures and therapy candidates with fewer side effects on the immune system and metabolism.

Source: DFG GEPRIS

TRR 152: Control of body homeostasis through TRP channel modules
Speaker: Prof. Dr. Thomas Gudermann
Institution: Walther Straub Institute of Pharmacology and Toxicology
Funding: since 2014

Website: Project description DFG
Topics: Transient receptor potential (TRP) channels represent an extended and diverse protein family fulfilling salient roles as versatile cellular sensors and effectors. The fundamental role of TRP channels in sensory processes has been highlighted by The Nobel Prize in Physiology or Medicine 2021. TRP proteins control an exceptionally broad spectrum of homeostatic physiological functions, illustrated by more than 20 hereditary human diseases caused by mutations in 14 Trp genes. Most TRP channel-related human disorders impinge on development, metabolism and other homeostatic functions. There is accumulating evidence to link TRP channels to even more human diseases beyond TRP channelopathies, and accordingly, TRP proteins have been identified as appealing therapeutic targets. Drawing on previous conceptual achievements and a unique TRP channel toolbox containing mouse models, specific antibodies, drug-like small molecules, and advanced experimental protocols, the CRC focuses on the overarching aim to validate TRP channels as new therapeutic targets. The following three challenges will be met: (1) There is a pressing need to further our understanding of the (patho)physiological role of TRP channels and their exact contribution to cellular, tissue and organismal homeostasis and dysfunction. (2) Applying new molecular approaches like single-particle cryo-electron microscopy along with advanced AI-based in silico methods, in-depth biophysical analyses, and medicinal chemistry, we will refine specific (photo-switchable) chemical probes to limit potential off-target and off-tissue side effects of drug-like small molecules. (3) To foster early clinical translation, reliable and robust pre-clinical disease models will be developed including genetically modified mouse models, in vitro human-derived organoids, and engineered human tissue. Three central questions will be addressed:(1)What are the building blocks of native TRP channels in defined tissues/cells and how do the components of TRP channel modules interact functionally in defined cellular compartments?(2)What is the physiological role of TRP channels in vivo and what is the precise mechanism of their activation and regulation?(3)What are the detailed pathomechanisms underlying human diseases caused by dysfunctional TRP proteins and which translational perspectives can be derived?Such fundamental insight will blaze the trail for specific, tailored treatment options for patients suffering from diseases inflicted by (dysfunctional) TRP proteins.

Source: DFG

Research groups with spokespersons

As an association of outstanding scientists, the research groups funded by the German Research Foundation (DFG) enable researchers to work on a joint research topic in a flexible network. The format is particularly suitable for opening up new subject areas and research directions.

Below you will find research groups in which the spokespersons are scientists at the LMU Faculty of Medicine.

FOR 5621: Development of a one-time gene therapy for age-related macular degeneration targeting CD146
Speaker: Prof. Dr. Stylianos Michalakis
Institution: Department of Ophthalmology
Funding: since 2024

Website: Project description DFG
Topic: Neovascular age-related macular degeneration (wet AMD) is a multifactorial disease leading to loss of central vision. It is the leading cause for blindness in the elderly western population and poses a significant clinical and economic burden. Implementation of anti-VEGF drugs like aflibercept, bevacizumab, ranibizumab and more recently brolucizumab in clinical practice has dramatically improved the prognosis of wet AMD. However, currently there is no cure for wet AMD and available treatments cannot prevent the development of atrophy and scar formation. Thus, it is mandatory to find new treatment options to address the unmet medical need in this devastating sight threatening disease. Here, we propose the development of a one-time gene therapy treatment of AMD based on a novel therapeutic target (CD146; gene name: MCAM). Different from previous approaches that directly inhibit the growth factor VEGFA, our approach targets both the proangiogenic and proinflammatory cell adhesion molecule CD146 to inhibit multiple signaling pathways crucially involved in the pathogenesis of AMD-related vision loss. Own preliminary results suggest that inhibition of CD146 reduces the formation of leaky choroidal blood vessels and the extent of lesion formation in the laser-induced choroidal neovascularization (CNV) mouse model of wet AMD. Previously, we generated variants of recombinant antibody fragments (Fabs) directed against mouse and human CD146 and confirmed high affinity binding to the extracellular domain of human CD146. In this project, we will further characterize the recombinant anti-CD146 Fabs and test dem for efficacy in relevant in vitro models and in the CNV mouse model of wet AMD. The most promising variants will then be produced as AAV-vectorized versions and tested again for in vitro and in vivo efficacy. In an alternative approach, we will generate and test AAV vectors expressing CRISPR-Cas9 and sgRNAs targeting the mouse Mcam gene for inactivation. Our overarching goal is to provide preclinical proof of concept for a novel, one-time gene therapy approach against wet AMD and to select an optimal candidate for future clinical translation.

Source: DFG

FOR 2879: ImmunoStroke - from immune cells to stroke recovery
Speaker: Prof. Dr. Arthur Liesz
Institution: Institute for Stroke and Dementia Research (ISD)
Funding: since 2019

Website: Description of the project GEPRIS
Themen: Ischemic stroke is the primary cause of long-term disability and the third leading cause of death in industrialized countries. Current treatments for stroke are limited, and preclinical experimental findings often fail in clinical trials. Therefore, new avenues of basic research with high translation potential are desperately needed in order to develop effective therapeutic strategies. Although the development of local inflammatory processes in the ischemic brain is a known phenomenon, precisely how these immune processes are linked to the secondary expansion of the infarct area and the role of the immune system in post-stroke regeneration remain poorly understood. Interestingly, while cerebral ischemia is traditionally not considered a classic neuroinflammatory disorder, stroke induces a plethora of immune responses similar to the responses that occur in autoimmune brain diseases. Moreover, the stroke-related acute brain injury has a robust effect on the peripheral immune system, inducing a multiphasic immune response. The reciprocal interaction between immunological responses and brain injury is poorly understood, particularly with respect to the mechanisms underlying recovery following stroke. This research unit ImmunoStroke which receives DFG-funding since 2019 is focusing on studying the role of immunity in repair mechanisms and long-term recovery following stroke. The projects described for the renewal of this consortium in its second funding period are designed to i) address how immunity modulates the recovery process following stroke; ii) clarify the role of neuroinflammation in stroke patients; and iii) and identify novel markers of post-stroke neuroinflammation. These goals will be achieved using cutting-edge technologies and new treatment paradigms in order to understand and modulate the immune responses that occur following experimental stroke. Importantly, the preclinical experiments will be highly standardized, the key findings will be validated in multicenter preclinical RCTs, and the experiments will be supported by analyses performed using stroke patients.

Source: DFG GEPRIS

DFG Clusters of Excellence, SFB and other DFG projects

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Clusters of Excellence with spokespersonship

Collaborative Research Centres with spokespersons

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