Alzheimerâ??s disease (AD)-related amyloid Beta-peptide (ABeta) pathology in the form of amyloid plaques and cerebral\namyloid angiopathy (CAA) spreads in its topographical distribution, increases in quantity, and undergoes qualitative\nchanges in its composition of modified ABeta species throughout the pathogenesis of AD. It is not clear which of\nthese aspects of ABeta pathology contribute to AD progression and to what extent amyloid positron emission\ntomography (PET) reflects each of these aspects. To address these questions three cohorts of human autopsy cases\n(in total n = 271) were neuropathologically and biochemically examined for the topographical distribution of ABeta\npathology (plaques and CAA), its quantity and its composition. These parameters were compared with\nneurofibrillary tangle (NFT) and neuritic plaque pathology, the degree of dementia and the results from\n[18F]flutemetamol amyloid PET imaging in cohort 3. All three aspects of ABeta pathology correlated with one another,\nthe estimation of ABeta pathology by [18F]flutemetamol PET, AD-related NFT pathology, neuritic plaques, and with the\ndegree of dementia. These results show that one aspect of ABeta pathology can be used to predict the other two,\nand correlates well with the development of dementia, advancing NFT and neuritic plaque pathology. Moreover,\namyloid PET estimates all three aspects of ABeta pathology in-vivo. Accordingly, amyloid PET-based estimates for\nstaging of amyloid pathology indicate the progression status of amyloid pathology in general and, in doing so, also\nof AD pathology. Only 7.75% of our cases deviated from this general association.
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