Matthew Moulton

Research into Alzheimer's disease (AD) has led to the identification of key molecular players in the etiology and pathogenesis of the disease. However, despite tremendous efforts, few effective therapeutic options are available for AD patients. In an effort to identify gene candidates that might prove useful for therapeutic intervention, I seek to better understand the molecular underpinnings of AD. Our lab has demonstrated that proper lipid generation and storage is critical for healthy brain function. While it is clear that under stress conditions, neurons produce lipids that are exported and endocytosed by glia to make lipid droplets (LDs), we do not know all the genes involved in this neuron-to-glia shuttling of lipids. I am undertaking an effort to identify these genes and examine their role in LD formation and clearance of the neurotoxic molecule Aβ42. Aβ42, a protein fragment produced by cleavage of APP, is lipophilic and we predict that it can be endocytosed through the same pathway used to endocytose lipids potentially leading to its sequestration and/or degradation. Thus, the formation of LDs may be beneficial in sequestering toxic species of lipids and proteins and an important pathway to consider for the development AD therapies.