Cerebral amyloid angiopathy distribution in older people: A cautionary note

Vafa Alakbarzade*, Jonathan M.R. French, David R. Howlett, Johannes Attems, Paul T. Francis, Sarah Stratton, Camilla N. Clark, Anthony C. Pereira, Atticus H. Hainsworth

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    10 Citations (Scopus)


    Introduction: Radiolabeled ligands for fibrillar amyloid beta (Aβ) peptides are used in positron emission tomography (PET) for dementia diagnosis. Current ligands do not discriminate parenchymal amyloid plaques from cerebral amyloid angiopathy (CAA). Methods: We undertook neuropathological examination of 65 older people (81.6 ± 7.96 (mean ± SD) years, 27F/38M): 15 with neuropathological diagnosis of AD, 25 with neuropathological diagnosis of other neurodegenerative dementias (Lewy body dementia and Parkinson disease dementia), and 25 without significant neurodegenerative pathology. Results: We observed CAA in non-Alzheimer's dementia (non-AD dementia) and control brains, of comparable extent to those with neuropathologically confirmed AD. Aβ-positive vessel density did not differ significantly between non-AD dementia and control groups. Across all subjects there was a highly significant correlation between vessel Aβ40 density and vessel Aβ42 density (Spearman rho = 0.855, P <.001). CAA was absent or sparse in subcortical white matter across all patient groups. Conclusion: Our data indicate that CAA can be abundant in non-AD brains and raise a cautionary note regarding interpretation of amyloid PET imaging.

    Original languageEnglish
    Article numbere12145
    JournalAlzheimer's and Dementia: Translational Research and Clinical Interventions
    Issue number1
    Publication statusPublished - 2021


    • Alzheimer's disease
    • amyloid PET
    • cerebral amyloid angiopathy


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