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Because current PET ligands underestimate nonfibrillar forms, we assayed soluble A\u03b2 in AD and controls. To identify the mechanisms responsible for soluble A\u03b2 in AD brains, we examined lipid rafts (LRs), where amyloid precursor protein (APP) is enzymatically processed. Frontal cortex was compared with cerebellum, which has minimal AD pathology. Compared with cognitively normal controls (CTL; Braak 0\u20101), elevations of soluble A\u03b240 and A\u03b242 were similar for intermediate\u2010 and later\u2010stage AD (Braak 2\u20103 and 4\u20106). Clinical\u2010grade AD showed a greater increase in soluble A\u03b240 than A\u03b242 relative to CTL. LR raft yield per gram AD frontal cortex was 20% below that of controls, whereas cerebellar LR did not differ by Braak score. The extensive overlap of soluble A\u03b2 levels in controls with AD contrasts with the PET findings on fibrillar A\u03b2. 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