Institute of Biochemistry and Pathobiochemistry
Biochemistry of Neurodegenerative Dieseases
Various approaches coming from neuropathology, genetics, animal modeling and biophysics have established a crucial role of protein misfolding in the pathogenic process of different neurodegenerative diseases, such as Alzheimer's disease, Parkinson’s disease, polyglutamine expansion diseases and prion diseases. However, there is an ongoing debate about the nature of the harmful proteinaceous species and how toxic conformers selectively damage neuronal populations.
The main aim of our biochemical research is to identify cellular factors and signaling cascades implicated in neuronal integrity and in the pathophysiological alterations leading to neurodegeneration. Our integrative research has a strong focus on the biochemical and cell biological analysis of cellular pathways, which are also of broad neurobiological interest. Specifically, we are employing in vitro, neuronal cell culture, and animal models to focus on four major topics:
Wu Z, Berlemann LA, Bader V, Sehr DA, Dawin E, Covallero A, Meschede J, Angersbach L, Showkat C, Michaelis JB, Münch C, Rieger B, Namgaladze D, Herrera MG, Fiesel FC, Springer W, Mendes M, Stepien J, Barkovits K, Marcus K, Sickmann A, Dittmar G, Busch KB, Riedel D, Brini M, Tatzelt J, Cali T, Winklhofer KF. (2022) LUBAC assembles a ubiquitin signaling platform at mitochondria for signal amplification and transport of NF-κB to the nucleus. EMBO J. 18: e112006. doi: 10.15252/embj.2022112006.
Polido SA, Kamps J, Tatzelt J. (2021) Biological Functions of the Intrinsically Disordered N-Terminal Domain of the Prion Protein: A Possible Role of Liquid-Liquid Phase Separation. Biomolecules 12; 11(8):1201. doi: 10.3390/biom11081201