## Abstract Positron emission tomography (PET) using [^11^C]PK 11195, a ligand for peripheral benzodiazepine receptor binding sites, offers the opportunity to image activated microglia in vivo. This tool may therefore be used to display the occurrence of microglial activation in the course of neuro
In vivo imaging of microglial activation with [11C](R)-PK11195 PET in corticobasal degeneration
✍ Scribed by Alexander Gerhard; Justin Watts; Iris Trender-Gerhard; Federico Turkheimer; Richard B. Banati; Kailash Bhatia; David J. Brooks
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 176 KB
- Volume
- 19
- Category
- Article
- ISSN
- 0885-3185
No coin nor oath required. For personal study only.
✦ Synopsis
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 ^11^C‐(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 ^11^C‐PK11195 binding in the caudate nucleus, putamen, substantia nigra, pons, pre‐ and postcentral gyrus, and the frontal lobe. __11__C‐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
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