== == Amyloid beta (AB) protein is produced from the cleavage of amyloid precursor protein (APP: a transmembrane protein) by beta secretase and gamma secretase. The build up of this intact AB protein leads to formation of amyloid plaques. Tau is a group of microtubule associated proteins which contributes to the assembly and stabilization of microtubules in axons. However, hyperphosphorylation of tau leads to tau aggregation and formation of neurofibrillary tangles (NFT). Intracellular NFT and extracellular amyloid plaques are two pathological hallmarks of Alzheimer's disease.

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In hereditary CAA, genetic defects, typically on chromosome 21, allow accumulation of amyloid, a protein made up of units called beta-pleated sheet fibrils. The fibrils tend to clump together, so that the amyloid cannot be dissolved.

Familial AD cases associated with presenilin mutations only account for a small proportion of AD cases. The physiological roles of presenilins are diverse and not completely understood. However, they play a role in the metabolism of the amyloid precursor protein (APP). Presenilin mutants are thought to decrease the metabolism of APP, but increase the proportion of specific amyloid beta (1-42) and truncated amyloid beta (x-42) alloforms. These types of proteins are prone to aggregate with one another, and form plaques (i.e., a common neurological hallmark of Alzheimer's disease). The pathological role of plaques and the intermediate stages in their formation is debated, however research suggests that smaller and more soluble amyloid beta aggregates are potent neurotoxins which may cause the initial stages of synaptic deterioration in disease.