A primary focus of our research is the neuronal mechanisms responsible for amyloid pathology and Alzheimer’s disease-related axonal transport defects. Here, we study APP metabolism, neuronal trafficking of APP and BACE1, and axonal transport dysfunction. The second focus of our research is to characterize the biological pathways and pathogenic mechanisms regulated by the second most common late-onset Alzheimer’s disease risk factor, BIN1. Here we employ a series of conditional knock-out and transgenic mouse models to characterize precisely how BIN1 acts as a risk factor to modify the synaptic function and tau pathology. Recently, we began to investigate molecular mechanisms underlying the interaction of amylin with Aβ pathology in order to explore the molecular link between type-2 diabetes and Alzheimer's disease. My group uses an integrated approach that combines hypothesis-driven mutagenesis, biochemical and pathological characterization, transcriptomics, proteomics, advanced live-cell imaging, superresolution microscopy, electrophysiology, and mouse behavior analysis to accomplish our goals. Cultured primary hippocampal neurons, microglia, and oligodendrocytes, established cell lines, hiPSC, transgenic mice, and conditional knockout mice serve as experimental models in our investigation.