Movement Disorders (revue)

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

Identifieur interne : 003C85 ( Main/Exploration ); précédent : 003C84; suivant : 003C86

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

Auteurs : Alexander Gerhard [Royaume-Uni] ; Justin Watts [Royaume-Uni, États-Unis] ; Iris Trender-Gerhard [Royaume-Uni] ; Federico Turkheimer [Royaume-Uni] ; Richard B. Banati [Royaume-Uni] ; Kailash Bhatia [Royaume-Uni] ; David J. Brooks [Royaume-Uni]

Source :

RBID : ISTEX:031BA769DE2642A0391D4654EF9922AA7CF66F48

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English descriptors

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

Url:
DOI: 10.1002/mds.20162


Affiliations:


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<div type="abstract" xml:lang="en">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</div>
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