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

Neurobiology of Disease

Hilary A. Archer¹  Alexander Hammers²  Nicola Pavese²  David J. Brooks³  Alexander Gerhard³  Federico E. Turkheimer⁴  Rainer Hinz⁵  Yen Fong Tai⁵  Martin Rossor⁵  Paul Edison⁵  Angus Kennedy⁵  Nick Fox⁵ 

[1] Corresponding author.;Wolfson Molecular Imaging Centre, The University of Manchester, UK;Dementia Research Centre, UCL, Institute of Neurology, Mainz, Germany;Hammersmith Imanet, GE Healthcare, Mainz, Germany;MRC Clinical Sciences Centre and Division of Neuroscience, Cyclotron Building Hammersmith Hospital, Imperial College London, W12 0NN, UK;

关键词: Alzheimer;    Amyloid;    Microglia;    PIB;    PK11195;    PET;   

DOI  :  

来源: DOAJ

【 摘 要 】

[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.

【 授权许可】

Unknown