individuals awaken, the production of beta-amyloid protein will be more consistent than its production during sleep. This is explained by two phenomena. The first is that the metabolic activity will be higher during waking, thus resulting in greater secretion of beta-amyloid protein. The second is that oxidative stress will also increase, which leads to greater AB production. On the other hand, it is during sleep that beta-amyloid residues are degraded to prevent plaque formation. The glymphatic system is responsible for this through the phenomenon of glymphatic clearance. Thus, during wakefulness, the AB burden is greater because the metabolic activity and oxidative stress are higher, and there is no protein degradation by the glymphatic clearance. During sleep, the burden is reduced as there is less metabolic activity and oxidative stress (in addition to the glymphatic clearance that occurs). Glymphatic clearance occurs during the NREM SWS sleep. This sleep stage decreases in normal aging, resulting in less glymphatic clearance and increased AB burden that will form AB plaques. Therefore, sleep disturbances in individuals with AD will amplify this phenomenon. The decrease in the quantity and quality of the NREM SWS, as well as the disturbances of sleep will therefore increase the AB plaques. This initially occurs in the hippocampus, which is a brain structure integral in long-term memory formation. Hippocampus cell death occurs, which contributes to diminished memory performance and cognitive decline found in AD. Although the causal relationship is unclear, the development of AD correlates with the development of prominent sleep disorders. In the same way, sleep disorders exacerbate disease progression, forming a positive feedback relationship. As a result, sleep disturbances are no longer only a symptom of AD; the relationship between sleep disturbances and AD is bidirectional. At the same time, it has been shown that memory consolidation in long-term memory (which depends on the hippocampus) occurs during NREM sleep. This indicates that a decrease in the NREM sleep will result in less consolidation, resulting in poorer memory performances in hippocampal-dependent long-term memory. This drop in performance is one of the central symptoms of AD. Recent studies have also linked sleep disturbances, neurogenesis and AD. The subgranular zone and the subventricular zone continued to produce new neurons in adult brains. These new cells are then incorporated into neuronal circuits and the subragranular zone, which is found in the hippocampus. These new cells contribute to learning and memory, playing an essential