1. Neuroinflammation, neuropil pathology, alterations of cerebral energy metabolism and glutamatergic neurotransmission in schizophrenia and affective disorders are a main focus of our research group.
The typical long-term course of schizophrenia and affective disorders with onset in early adulthood, progressive as well as benign courses, exacerbations and remissions, shows similarities to various autoimmune disorders (e.g., multiple sclerosis, psoriasis, myasthenia gravis) and leads to the speculation of similar pathogenetic components. In addition to a well established neurodevelopmental component in the pathogenesis of schizophrenia, several MRI-studies reported a subtle progressive loss of brain tissue. This reduction of brain tissue without indications of neuronal loss seems to be caused by degenerative changes of neuropil or glial cells. In addition, several lines of evidence suggest that alterations in cerebral energy / glucose supply – which are closely linked with disturbances in glutamatergic neurotransmission – are another important factor which may contribute to the disease progression. All these pathophysiological components were shown to be closely interlinked.
Using whole-brain sections from the Magdeburg Brain Collection (Prof. B. Bogerts), marker-proteins for neuroinflammatory processes, disturbances in myelination, cerebral energy metabolism and glutamatergic neurotransmission are investigated in brains from patients with schizophrenia / affective disorders and normal controls.
In addition, blood samples from acutely ill and remitted patients with schizophrenia and affective disorders are analyzed for immunological changes in cooperation with the Institute of Experimental Immunology, EUROIMMUN, Lübeck (Prof. W. Stöcker) and the Department of Clinical Immunology & Rheumatology, Medical School Hanover (Prof. R. Jacobs) |