Microglia, amyloid, and cognition in Alzheimer's disease: An [11C](R)PK11195-PET and [11C]PIB-PET study

Paul Edison, Hilary A. Archer, Alexander Gerhard, Rainer Hinz, Nicola Pavese, Federico E. Turkheimer, Alexander Hammers, Yen Fong Tai, Nick Fox, Angus Kennedy, Martin Rossor, David J. Brooks

    Research output: Contribution to journalArticlepeer-review


    [11C](R)PK11195-PET is a marker of activated microglia while [11C]PIB-PET detects raised amyloid load. Here we studied in vivo the distributions of amyloid load and microglial activation in Alzheimer's disease (AD) and their relationship with cognitive status. Thirteen AD subjects had [11C](R)PK11195-PET and [11C]PIB-PET scans. Ten healthy controls had [11C](R)PK11195-PET and 14 controls had [11C]PIB-PET scans. Region-of-interest analysis of [11C](R)PK11195-PET detected significant 20-35% increases in microglial activation in frontal, temporal, parietal, occipital and cingulate cortices (p <0.05) of the AD subjects. [11C]PIB-PET revealed significant two-fold increases in amyloid load in these same cortical areas (p <0.0001) and SPM (statistical parametric mapping) analysis confirmed the localisation of these increases to association areas. MMSE scores in AD subjects correlated with levels of cortical microglial activation but not with amyloid load. The inverse correlation between MMSE and microglial activation is compatible with a role of microglia in neuronal damage. © 2008 Elsevier Inc. All rights reserved.
    Original languageEnglish
    Pages (from-to)412-419
    Number of pages7
    JournalNeurobiology of disease
    Issue number3
    Publication statusPublished - Dec 2008


    • Alzheimer
    • Amyloid
    • Microglia
    • PET
    • PIB
    • PK11195


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