Mutations in the progranulin gene (GRN) lead to the development and progression of the neurodegenerative disease, frontotemporal lobar degeneration (FTLD). Progranulin is a secreted protein that is widely expressed throughout the body and is important for regulating inflammation and cell stress responses. In the brain, progranulin is expressed in only two cell types, neurons and microglia. Functionally, progranulin is thought to help regulate lysosome function, which is important for clearing the cell of old or defective organelles and toxic proteins, prevents neurodegeneration, and promotes cell survival. Mutations in the GRN gene that cause FTLD lead to reduced progranulin levels in the brain, the toxic build-up of a nuclear RNA-binding protein, TDP-43, in neurons, increased microglial inflammatory responses, and neuronal cell death. Currently, there are no known cures for FTLD. Cell models with measurable phenotypes that accurately model the human disease are powerful tools for the identification of new treatments. Human cell models based on patient-derived induced pluripotent stem cells (iPSCs) may have greater relevance and improved translation than non-human models. Phenotypic screening with cell-based disease models has led to more first-in-class drugs than other strategies that rely solely on target-based approaches. In order to create potential new treatments for FTLD, we propose to differentiate iPSCs from human FTLD patients into neurons and microglia, and identify robust phenotypes using our robotic microscopy imaging technology to develop cell models that can be used to screen for new drug targets to treat FTLD.