Tau dysfunction is implicated in many neurodegenerative diseases, including Alzheimer’s disease, frontotemporal dementia, progressive supranuclear palsy, corticobasal degeneration, and Pick’s disease. Most of these diseases are characterized by tau protein aggregation and are termed tauopathies. In these diseases, tau is affected at the molecular (splicing), protein (hyperphosphorylation, cleavage, aggregation), and cellular (secretion) levels. The goal of the Karch lab is to understand the molecular and cellular mechanisms underlying tauopathies. Defining the molecular mechanisms underlying tauopathies requires unraveling the complexities of the MAPT gene that encodes the tau protein, tau protein dysfunction within the cell, and the cell-cell interactions that produce pathology in the human brain. We use traditional immortalize and primary culture models in combination with human induced pluripotent stem cell-derived neuron and astrocytes. Defining the molecular and cellular mechanisms underlying tauopathies will improve our understanding of how tau genetics influences tau biology and will inform novel avenues for therapeutic intervention.


 tuj 10x  a copy  MN Diff TUJ + H a 20x copy ChAT + TUJ + H GFAP + dapi 20x  b copy