In Vivo Mapping of Vascular Inflammation Using the Translocator Protein Tracer 18F-FEDAA1106

Simon Cuhlmann, Willy Gsell, Kim Van der Heiden, Josef Habib, Jordi L Tremoleda, Magdy Khalil, Federico Turkheimer, Merlijn J Meens, Brenda R Kwak, Joseph Bird, Anthony P Davenport, John Clark, Dorian Haskard, Rob Krams, Hazel Jones, Paul C Evans

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)


Noninvasive imaging methods are required to monitor the inflammatory content of atherosclerotic plaques. FEDAA1106 (N-(5-fluoro-2-phenoxyphenyl)-N-(2-(2-fluoroethoxy)-5-methoxybenzyl) acetamide) is a selective ligand for TSPO-18kDa (also known as peripheral benzodiazepine receptor), which is expressed by activated macrophages. We compared 18F-FEDAA1106 and 2-deoxy-2-[18F]fluoro-d-glucose (18F-FDG, a marker of glucose metabolism) for positron emission tomographic (PET) imaging of vascular inflammation. This was tested using a murine model in which focal inflammation was induced in the carotid artery via placement of a constrictive cuff. Immunostaining revealed CD68-positive cells (macrophages) at a disturbed flow site located downstream from the cuff. Dynamic PET imaging using 18F-FEDAA1106 or 18F-FDG was registered to anatomic data generated by computed tomographic (CT)/CT angiography. Standardized uptake values were significantly increased at cuffed compared to contralateral arteries using either 18F-FEDAA1106 (p < .01) or FDG (p < .05). However, the 18F-FEDAA1106 signal was significantly higher at the inflamed disturbed flow region compared to the noninflamed uniform flow regions, whereas differences in FDG uptake were less distinct. We conclude that 18F-FEDAA1106 can be used in vivo for detection of vascular inflammation. Moreover, the signal pattern of 18F-FEDAA1106 corresponded with vascular inflammation more specifically than FDG uptake.
Original languageEnglish
Pages (from-to)1-10
Number of pages10
Issue number0
Publication statusPublished - 2014


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