Our Research
Our lab investigates the mechanisms that regulate Alzheimer’s disease (AD) pathogenesis and neuronal dysfunction. Our lab has made outstanding contributions to our understanding of amyloid precursor protein (APP) trafficking and the biology of BACE1 and γ-secretase, the two enzymes that sequentially cleave APP to generate Aβ. I led a research group at the University of Chicago for twenty years, investigating multiple aspects of AD cell biology and molecular neuropathology. In 2019, I moved to the University of South Florida to become the Associate Dean of Neuroscience Research and the CEO of the Byrd Alzheimer’s Center and Research Institute. Over the years, our research has provided valuable insights into the regulation of APP trafficking and metabolism, the modulation of Aβ production and deposition through post-translational modifications of APP secretases, and the neuronal transcytosis of BACE1.
In recent years, we have characterized late-onset AD risk factors identified through GWAS efforts using cell-type-specific conditional knock-out and transgenic mice. We have published key findings on BIN1 as a risk factor for tau pathogenesis, on the function of microglial BIN1 in neuroinflammation, and on the neuronal BIN1 interactome. More recently, we have also contributed to research on the microglial functions of the PICALM AD risk allele and the regulation of neuron-glia communication by CLU.
