Dieter Edbauer

Prof. Dr. Dieter Edbauer serves as Group Leader at the German Center for Neurodegenerative Diseases (DZNE) in Munich, where he leads research focused on Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) pathogenesis. His laboratory investigates the molecular mechanisms underlying C9orf72-related neurodegenerative diseases, with particular emphasis on dipeptide-repeat (DPR) proteins and their role in disease progression.

Dr. Edbauer's research program centers on understanding how C9orf72 repeat expansions lead to neurodegeneration through the production of toxic dipeptide-repeat proteins. His team discovered that the (GGGGCC)n repeat in C9orf72 is translated into aggregating DPR proteins despite being intronic and lacking an ATG start codon. Current research examines how these proteins trigger TDP-43 pathology, exploring mechanisms from ultrastructural changes to patient-level manifestations. His work spans multiple approaches including cellular models, mouse studies, proteomics, and cryo-electron tomography to develop potential therapeutic interventions targeting DPR synthesis or toxicity.

Dr. Edbauer's publications reveal a consistent research trajectory investigating the fundamental mechanisms of C9orf72 ALS/FTD, with particular focus on DPR protein biology, cellular transmission mechanisms, and connections to TDP-43 pathology. His work bridges basic molecular mechanisms with potential clinical applications, particularly in developing biomarkers and immunotherapeutic approaches.

His research is supported by significant funding from prestigious organizations:

• European Research Council (ERC)
• NOMIS Foundation
• SyNergy Cluster of Excellence (DFG)

Dr. Edbauer maintains active collaborations with multiple institutions including the Max Planck Institute in Martinsried (for proteomics and cryo-electron tomography) and clinical partners at DZNE Munich for human tissue validation. His laboratory employs a multidisciplinary approach combining primary neuron culture, mouse models, and advanced imaging techniques to dissect C9orf72 pathogenesis from molecular mechanisms to potential therapeutic interventions.