Alzheimer’s disease (AD) is a neurodegenerative disorder that affects roughly 11% of Americans over the age of 65. So far, treatment has only been successful at reducing visible symptoms of AD, but unfortunately lack the capacity to slow or stop the progression of disease. Drosophila melanogaster have proven to be successful research models of neurodegeneration in the brain; they possess a nervous system that significantly resembles that of humans, most importantly the existence of the blood brain barrier (BBB), which is an important structure to consider for modeling mechanisms of treatment delivery across the BBB. It has been used to model neurodegenerative diseases such as Parkinson’s Disease and other neurodegenerative diseases of the central nervous system (CNS). Since the literature supports treatment with scopolamine in mouse models induces Alzheimer’s-like clinical presentations, we propose that a scopolamine-induced AD in a Drosophila model would sufficiently mimic the human neuropathogenesis of AD. Here, wild-type Drosophila are to be treated with scopolamine to induce Alzheimer’s-like disease progression. Male and female cohorts will be followed post-scopolamine treatment to monitor its effects on the nervous system and the progression of the disease model. Rapid Iterative Negative Geotaxis (RING) assays and courtship assays will be performed to continually monitor neurodegenerative changes in motor function and short-term memory, respectively. We predict that if scopolamine-treated Drosophila melanogaster is to be a successful model of AD, that the treatment cohorts will express a progressively decreasing motor function as well as a reduced ability to maintain short-term memory loss when compared to controls.