The formation of amyloid plaques begins with the cleavage of amyloid precursor protein (APP) by β-secretase and γ-secretase enzymes. This process generates Aβ peptides, which aggregate to form oligomers, fibrils, and eventually plaques. The Aβ aggregates are toxic to neurons, leading to synaptic dysfunction and neuroinflammation, which are critical events in the pathogenesis of AD.
