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Microglial imaging with positron emission tomography and atrophy measurements with magnetic resonance imaging in multiple sclerosis: a correlative study

Division of Nuclear Medicine, Ghent University Hospital, Ghent, the Netherlands, Department of Biological Psychiatry, University Hospital, Groningen, the Netherlands

J C Debruyne

Department of Neurology, Ghent University Hospital, Ghent, the Netherlands, jan.debruyne{at}UGent.be

K J Van Laere

Division of Nuclear Medicine, Ghent University Hospital, Ghent, the Netherlands

F De Vos

Laboratory of Radiopharmacy, Ghent University, Ghent, the Netherlands

J Keppens

Division of Nuclear Medicine, Ghent University Hospital, Ghent, the Netherlands

K Strijckmans

Laboratory of Analytical Chemistry, Institute for Nuclear Sciences, Ghent University, Ghent, the Netherlands

E Achten

Department of Radiology, MR-Unit, Ghent University Hospital, Ghent, the Netherlands

G Slegers

Laboratory of Radiopharmacy, Ghent University, Ghent, the Netherlands

R A Dierckx

Division of Nuclear Medicine, Ghent University Hospital, Ghent, the Netherlands

J Korf

Department of Biological Psychiatry, University Hospital, Groningen, the Netherlands

J L De Reuck

Department of Neurology, Ghent University Hospital, Ghent, the Netherlands

Objective: The objectives of the present study were to assess brain atrophy in multiple sclerosis (MS) patients during different disease stages and to investigate by PET and [¹¹C]PK11195, a marker of microglial activation, the relationship between inflammation, atrophy and clinically relevant measures. Methods: Eight healthy subjects and 22 MS patients were included. Semiquantitative [¹¹C]PK11195 uptake values, with normalization on cortical grey matter, were measured for magnetic resonance imaging T₂- and T₁-lesions and normal appearing white matter (NAWM). As atrophy index we used the ratio of the amount of white and grey matter divided by the ventricular size, using an optimized a priori based segmentation algorithm (SPM99). Results: Atrophy was significantly greater in MS patients compared to age-matched controls. A significant correlation was found between brain atrophy and both disease duration and disability, as measured with the Expanded Disability Status Scale. For NAWM, [¹¹C]PK11195 uptake increased with the amount of atrophy, while T₂-lesional [¹¹C]PK11195 uptake values decreased according to increasing brain atrophy. Conclusions: The present study suggests that brain atrophy, correlating with disease duration and disability, is directly related to NAWM and T₂-lesional inflammation as measured by microglial activation.

Key Words: atrophy • [11C]PK11195 • inflammation • microglia • multiple sclerosis • positron emission tomography

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