Events
QB3 Webinar: Martin Kampmann, UCSF
Protein aggregation in neurons plays a critical role in Alzheimer’s disease and related dementias. What controls this aggregation and why is it toxic? Why are certain neuron types vulnerable? And how do microglia, astrocytes, and oligodendrocytes contribute to disease? These are questions Martin Kampmann’s lab at UCSF is addressing with new technologies. Their ultimate goal: to discover new therapeutic strategies. Join us September 18 to learn how Kampmann and his lab have pioneered CRISPR-based screens in patient-derived cells and mouse models, and how they use biochemistry, biophysics and cell biology to test hypotheses generated by their functional genomics platform.
Register for the Livestream
About the Speaker
The Kampmann lab develops and applies innovative technologies to understand cellular and molecular mechanisms of aging-associated neurodegenerative diseases, and to discover new therapeutic strategies. A major focus of our research are Alzheimer’s disease and related dementias.
The lab has pioneered CRISPR-based screens in human iPSC-derived neurons, glia and 3D assembloids, which enables unbiased discovery of disease-relevant cell biology in patient-derived cells. We have also developed scalable cell type-specific CRISPR screening approaches for mouse models of disease.
We use biochemistry, biophysics and cell biology to test mechanistic hypotheses generated by our functional genomics platform.
Major research questions are:
- What controls protein aggregation in neurons? Why is it toxic and how does it affect neuronal and synaptic function? Why are some neuronal subtypes selectively vulnerable? Our main focus here is on the protein tau.
- How do non-neuronal cells such as microglia, astrocytes, and oligodendrocytes contribute to disease? What controls their beneficial and toxic states and functions in disease?
