Volume 19, Issue 10 p. 1221-1226
Brief Report

In vivo imaging of microglial activation with [11C](R)-PK11195 PET in corticobasal degeneration

Alexander Gerhard MD

Corresponding Author

Alexander Gerhard MD

MRC Clinical Sciences Center and Division of Neuroscience, Faculty of Medicine, Imperial College, London, United Kingdom

MRC Cyclotron Building, Hammersmith Hospital, Du Cane Rd., London W12 0NN United KingdomSearch for more papers by this author
Justin Watts MS

Justin Watts MS

MRC Clinical Sciences Center and Division of Neuroscience, Faculty of Medicine, Imperial College, London, United Kingdom

Emory University School of Medicine, Department of Neurology, Atlanta, Georgia, USA

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Iris Trender-Gerhard MD

Iris Trender-Gerhard MD

Institute of Neurology, Queen Square, London, United Kingdom

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Federico Turkheimer PhD

Federico Turkheimer PhD

MRC Clinical Sciences Center and Division of Neuroscience, Faculty of Medicine, Imperial College, London, United Kingdom

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Richard B. Banati MD

Richard B. Banati MD

MRC Clinical Sciences Center and Division of Neuroscience, Faculty of Medicine, Imperial College, London, United Kingdom

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Kailash Bhatia MD

Kailash Bhatia MD

Institute of Neurology, Queen Square, London, United Kingdom

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David J. Brooks MD, DSc

David J. Brooks MD, DSc

MRC Clinical Sciences Center and Division of Neuroscience, Faculty of Medicine, Imperial College, London, United Kingdom

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First published: 20 May 2004
Citations: 121

Abstract

Corticobasal degeneration (CBD) is a neurodegenerative parkinsonian disorder of unknown cause that shows considerable clinical heterogeneity. In CBD, activated microglia have been shown to be associated closely with the extensive tau pathology found in the affected basal ganglia, brainstem nuclei, and cortical regions. We report on the use of [11C](R)-(1-[2-chlorophenyl]-N-methyl-N-[1-methylpropyl]-3-isoquinoline carboxamide) (PK11195) positron emission tomography (PET), a marker of peripheral benzodiazepine binding sites (PBBS) that are expressed by activated microglia, to demonstrate in vivo the degree and distribution of glial response to the degenerative process in 4 patients with CBD. Compared with normal age-matched controls, the CBD patient group showed significantly increased mean [11C](R)-PK11195 binding in the caudate nucleus, putamen, substantia nigra, pons, pre- and postcentral gyrus, and the frontal lobe. [11C](R)-PK11195 PET reveals a pattern of increased microglial activation in CBD patients involving cortical regions and the basal ganglia that corresponds well with the known distribution of neuropathological changes, which may therefore help to characterize in vivo the underlying disease activity in CBD. © 2004 Movement Disorder Society