Public Health & Health Science Division, ULAB

Dysregulated sleep is often a typical companion of Alzheimer’s disease and other forms of dementia, but the exact relationship between the two remains complex. Beta-amyloid (Aβ) is a protein related to the onset of dementia, with high levels of Aβ plaque buildup being positively correlated with Alzheimer’s disease, but it is unclear by which mechanism Aβ causes dementia. Recent studies have suggested a bidirectional relationship between sleep disturbances and Alzheimer's pathology, wherein disrupted sleep may prevent the clearing of Aβ plaque from the extracellular space, thus exacerbating Aβ accumulation and vice versa, creating a cycle that accelerates cognitive decline. Continuously activated microglia may play a role in the development of neurodegenerative diseases. Microglia are the main sources of brain inflammation, and thus, research indicates that excessively activated microglia can generate elevated levels of proinflammatory cytokines and chemokines, which are neuroimmune inflammatory factors that ultimately result in impaired neuronal function. The emphasis on early disease stages is pivotal in highlighting treatments targeting later stages as well, particularly dementia. While addressing early stages is crucial, it is just as important to address and develop symptomatic treatments for advanced disease stages. Our research highlights various approaches to addressing the various stages of Alzheimer's disease. Current studies focusing on non-pharmacological prevention are increasingly utilizing evidence-based multimodal intervention programs that coincide with lifestyle changes and sleeping habits. Other pharmaceutical therapies including drugs that target Aβ plaque and others that modulate neuroinflammatory pathways are also being implemented. In addition, immunotherapy has also proven to be useful as it employs both active and passive strategies in formulating anti-beta-amyloid antibodies. Our analysis and research seek to combine various methods of interventions to mitigate AD while seeking to find improved study designs for more effective preventive outcomes.