Our lab is interested in the cellular and molecular changes that serve as the basis for Alzheimer’s disease (AD) and the systems that result in neuronal death and cognitive decline. We work with a variety of models: Drosophila melanogaster, human cell lines, and humanized mouse astrocytes. There is a high degree of phenotypic conservation among human patients and these models, so they serve as useful modes of investigating the causes and progression of neurodegenerative disease. Our focus is on the earliest changes that cells experience before they begin their decline. We are interested in modulating the effects of AD through a metabolic lens. Mutations in the Presenilin (Psn) gene are the most common cause of early onset AD, so we use Psn knockdown models in Drosophila to assess the level of impairment. We believe that studying the early-stage changes that contribute to the progression of AD, such as gene expression changes that lead to alterations in autophagy, mitochondrial size and function, and lipid metabolism, will provide insight into the functional mechanisms of AD and lead us to the development of a pharmaceutical target.