Alzheimer's Disease (AD) is one of the most common forms of neurodegenerative disease characterized by progressive cognitive decline. The pathogenesis of AD is complex and remains elusive. The disease is marked by progressive deposition and accumulation of extracellular ß-amyloid (Aß), and aggregation of intracellular Tau proteins in the brain, leading to neuronal death and cognitive impairment. However, the amyloid cascade hypothesis is widely acknowledged, especially following the recent approval of anti-amyloid antibodies for AD treatment.

Figure 1. Mechanisms of Aß deposition and Tau protein aggregation leading to neurologic dysfunction and degeneration in AD[1]