We are interested in the pathological alterations in neurodegenerative diseases, in particular in Parkinson disease. During the last decade considerable progress has been made with respect to the genetic basis of the disease. Several genetic factors have been identified that are associated with Parkinson disease, and the biological pathways leading to pathology are under intense investigation. Besides the degeneration of dopamine neurons in the midbrain and depletion of striatal dopamine levels, we know that other cells undergo pathological changes in the brain and in peripheral organs including the gut.
- We study genetic risk factors linked to monogenetic forms of Parkinson disease both in postmortem human patient material and model systems. Many of the mutant genes are involved in mitochondrial or lysosomal functions. In collaboration with other research groups we use rodent models carrying these mutations to explore the mechanisms leading to degeneration.
- We also study the development of motor and non-motor symptoms in a genetic mouse model of Parkinson disease, the MitoPark mouse. These mice, which mimic mitochondrial failure in dopamine neurons detected in Parkinson patients, develop slowly progressing motor impairments and gut disturbances. At different ages mice can be used to test novel treatment strategies for patients in early, middle and late stages of the disease. Different variants of the MitoPark line are used to study the role of glia cells in Parkinson disease.
We combine behavioral tests with biochemical and histological methods to study molecular alterations in distinct brain areas or cell populations affected in the brain and gastro-intestinal tract. A detailed understanding of pathological alterations in the central and enteric nervous system associated with Parkinson’s disease will possibly pave the way for future therapies for neurodegeneration, targeting also glia cells.
Dagmar Galter - Associate Professor
Sandra Gellhaar - Postdoc
Kristina Langemack - PhD student