There are 40 million people worldwide living with Alzheimer's Disease (AD), and by 2050 the prevalence is expected to increase to 150 million people, thus resulting in a 1 in 2 chance of having AD by the age of 85. An increase in amyloid-b plaques (Ab) and hyperphosphorylated tau are widely accepted as the core indicators of the disease. These indicators of AD onset and progression are becoming increasingly attributed to the disturbance of optimal sleep/wake cycles. Additionally, AD progression exacerbates normal sleep/wake cycles, resulting in a cyclical worsening of AD pathology, circadian rhythm, and cognitive dysfunction. By using an Ab intracerebroventricular (ICV) injection mouse model, mice can present an AD-like pathology within days to weeks after injection, allowing for the expedited examination of the disease. This model can serve as a tool to investigate the mechanism behind the disturbance of the biological clock and AD progression, and therefore find therapeutic targets to delay, prevent or cure the disease.