Dementia is a global health challenge, with an estimated 55 million individuals globally, projected to increase to 152 million by 2050. The leading cause of dementia is Alzheimer’s disease (AD), a neurodegenerative disease accounting for 60–70% of all dementia cases. There is an urgent need for a therapeutic breakthrough that stops and even reverses the cognitive decline in a broad range of AD patients. Since cognitive functions arise from the interactions between many neurons organised in circuits, the central question of this project is how AD-induced abnormalities in individual neurons eventually impair the function of the embedding circuits. We hypothesise that neural hyperexcitability contributes to the pathogenesis of cognitive impairments in early-stage AD. Toxin aggregates trigger neural hyperexcitability but escalate by a deficit in homeostatic plasticity during sleep. This project aims to establish the scientific evidence of the neural plasticity mechanism in people with early AD and then demonstrate a neuromodulation strategy to ameliorate it. It involves a stepwise experiment that includes two studies with repeated measurements of neural activity during sleep, neural excitability, and cognitive performance before and after in a cohort of people with early-stage AD. We will also use novel non-invasive brain stimulation technology to augment the neural activity during sleep that is known to have a homeostatic plasticity effect, first acutely and then repeatedly over days. If successful, the project will elucidate a pathogenesis mechanism in the early stages of AD that is critical for developing clinically meaningful therapies and demonstrate the feasibility of a neuromodulation therapeutic strategy.