Investigation of protein misassembly, misfolding or misprocessing in brain diseases, and the development of pharmacotherapies to interfer with or prevent these protein pathologies. There is a focus on neurobiology and proteinbiochemistry. Generation of (mis)assembled proteins is investigated at the levels of generation, recognition and degradation in in vitro and in vivo models.
1. Neurobiology of chronic mental illnesses (CMI) like schizophrenia and recurrent affective disorders. Identification and characterization of CMI-associated proteins by proteomics, biochemistry, cell biology. Characterizing sporadic CMI as protein misassembly disorders. Development of animal models for CMI.
2. Translational research for redefining purely clinical diagnoses based on self-reporting by biological correlates. Identifying biological markers as diagnostic tests for schizophrenia.
Interview of International Innovation with Carsten Korth from July 2012 on Mental illness Research: 2012_Interview_CK Format: PDF, 536 KB
3. Development of animal models for protein conformational disorders. See here a 5 minute film clip of our transgenic animal model for early Alzheimer’s disease expressing exclusively Abeta dimers and displaying cognitive deficits and depressive-like behaviour (Müller-Schiffmann, 2015).
4. Cell biology and functional regulation of protein misfolding. Generation of conformation-sensitive ligands, monoclonal antibodies and recombinant antibodies for disgnosing and characterizing protein conformational diseases, in particular prion-protein associated diseases and Alzheimer's disease. Development of animal models for protein conformational disorders.
5. Pharmacotherapy of protein conformational diseases. Using prion protein conformers and Abeta oligomers as models, neutralizing chimeric small molecules and recombinant antibody fragments have been and are currently developed that target specific, toxicity-associated conformations.
6. Neurobiology of Aging. Insoluble and aggregated protein deposits are not only hallmarks of neurodegenerative disorders but are also hallmarks of the aging brain in the form of acculumating lipofuscin and other cellular debris. Dysfunctional protein degradation in the aging post-mitotic cell is investigated by proteomic, biochemical and cell biological techniques. Cross-influences to protein conformatonal diseases are revealed.