I am an A.P. Giannini postdoctoral fellow in Martin Kampmann’s lab at UCSF where I am utilizing my expertise in epigenetics and genetic screens to discover molecular and cellular mechanisms relevant to neurodegeneration.Alzheimer’s disease and related dementias are widely known as proteinopathies, where protein misfolding and eventual aggregation are considered the root cause of cellular dysfunction and disease. While it is clear that misprocessed proteins such as tau play causal roles in disease, the exact molecular mechanisms that lead to this misprocessing and ultimately neurodegeneration are largely unknown. Tau is likely pathogenic well before it becomes filamentous aggregates (or fibrils), and understanding how these pathogenic versions of tau influence cellular function could be key to understanding disease-causing mechanisms.In the Kampmann lab, I am using stem-cell derived neurons with MAPT mutations to model disease. I am especially interested in uncovering how mutant tau influences chromatin and RNA states and how that drives disease-relevant cellular phenotypes. I am developing CRISPR-based genetic modifier screens to address these mechanisms directly. In addition to these efforts, I have a long-term interest in DNA methylation and RNA methylation and their relationship to aging and neurodegeneration.