In Alzheimer's disease, the amyloid precursor protein is cleaved, or "cut," to form small proteins known as Aβ. Once formed, Aβ stimulates refolding of more Aβ peptides, which then assemble into amyloid fibers that form plaques (shown below). In patients with AD, Aβ prions appear to begin multiplying deep in the temporal lobes of the brain and then spread to other regions.
Aβ also stimulates the misfolding of another protein called tau. Misfolded tau assembles into fibers that condense inside neurons to form tangles.
Plaques and tangles are the pathological hallmarks of AD.