Alzheimer’s disease (AD) is a neurodegenerative pathology clinically characterized by cognitive decline and changes in behavior and personality. BACE1 is the sole enzyme responsible for cleaving amyloid precursor protein (APP) to initiate the production of beta amyloid (Ab) peptides and oligomers in AD. Some studies propose that high BACE1 levels in AD are due to alteration of its metabolism as a consequence of abnormal cellular trafficking and sorting. Recently, the Tesco Lab described that GGA3 adaptor protein can modulate BACE1 trafficking to the lysosome. My project focuses on BACE1 trafficking to axons and dendrites in neuronal cultures models using a live cell imaging approach.