We are utilizing hiPSC cells to model Parkinson’s disease (LRRK2 G2019S-mutation). My focus is in PD related neuroinflammation and glial cells, microglia and astrocytes.
Our primary disease models are transgenic mice carrying familial Alzheimer or frontotemporal dementia linked human APP, PSEN1 and tau mutations. These mice with highly predictable time course of pathology progress allow us to study the very first steps in the disease pathogenesis in the brain, whereas neuropathological examination in human patients is usually limited to the advanced cases.
To test the disease mechanisms, we perform intervention with special diets, pharmacological agents, antibodies and viral vector mediated gene transfer or cross these mice expressing typical Alzheimer pathology with a mouse line carrying a gene defect that potentially modulate the main pathology.
To directly study the brain functions, we use multichannel and multisite electrophysiological recording in freely moving (or sleeping) mice alone or combined with functional MRI or PET in collaboration with the Biomedical Imaging group. In addition, we conduct a large battery of behavioral tests to assess memory functions, emotionality, social behavior as well as motor and sensory functions.
At the end of any study, the mouse brain is carefully examined for hallmarks of AD pathology (amyloid deposit, tau phosphorylation, neuroinflammation) and other processes of interest. Here we apply light, fluorescent and confocal microscopy and combine these with gene expression or protein assays from brain and if needed from other tissue.
I lead the Neuroinflammation research group. We aim to find regulators of microglial dysfunctions in neurodegenerative diseases.
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