The Pathogenesis of Alzheimer's Disease: A Reevaluation of the “Amyloid Cascade Hypothesis”

Table 1

Molecular composition of β-amyloid (Aβ) deposits in Alzheimer’s disease (AD).

Deposit subtype	Molecular composition
Diffuse Aβ	APP (lacking C terminus), Aβ 42/43 apolipoprotein E, α 1-antichymotrypsin, HSPG, complement proteins (C1q, C3, C4), amyloid-P
Primitive Aβ	APP (N & C-terminal), Aβ 42/43, free and conjugated ubiquitin, PHF antigen, phosphorylated tau, chromogranin-A, bFGF, apolipoprotein E, interleukin-6
Classic Aβ	Aβ 42/43 “core”, α-synuclein “ring”, Aβ 40, actin, tubulin, phosphorylated tau, NF-protein, CAM, chromogranin-A “ring”, α 2-macroglobulin, complement proteins “core”, immunoglobulins “core”, amyloid-P, α 1-antichymotrypsin, antitrypsin, antithrombin III, apolipoprotein E and D “core”, bFGF, PrP, silicon/aluminium “core”, interleukin-6 “ring”

Aβ: β-amyloid, APP: amyloid precursor protein, bFGF: basic fibroblast growth factor, CAM: cell adhesion molecule, HSPG: heparan suphate proteoglycan, NF-protein: neurofilament protein, PHF: paired helical filament, and PrP: prion protein.