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Abstract #2909

Disentangling apparent discordance between ASL-MRI and [18F]-FDG PET following a single dose of the β2-agonist clenbuterol

Courtney A. Bishop1, Gaia Rizzo1, Thomas Lodeweyckx2, Jan de Hoon2, Koen Van Laere3,4, Michel Koole4, Wim Vandenberghe5, Eugenii Rabiner1,6, Renee Martin7, Anthony Ford7, and Gabriel Vargas7
1Invicro, London, United Kingdom, 2Center for Clinical Pharmacology, Department of Pharmaceutical and Pharmacological Sciences, KU Leuven, Leuven, Belgium, 3Division of Nuclear Medicine, University Hospital Leuven, Leuven, Belgium, 4Nuclear Medicine and Molecular Imaging, KU Leuven, Leuven, Belgium, 5Department of Neurology, University Hospital Leuven, Leuven, Belgium, 6Centre for Neuroimaging Sciences, Institute of Psychiatry, Psychology and Neuroscience, King’s College, London, United Kingdom, 7CuraSen Therapeutics, San Carlos, CA, United States


Here we demonstrate that an apparent discrepancy in CBF (from ASL) and CMRglu (from [18F]-FDG PET) following high-dose administration of clenbuterol in healthy volunteers is caused by within-scan rising plasma glucose concentrations. With simulation-based correction, post-clenbuterol CBF changes from ASL agree with blood flow estimates from [18F]-FDG PET, without increase in CMRGlu. ASL-MRI may therefore provide a valuable tool for monitoring the central effects of β2-adrenergic receptor activation in larger, future studies on both healthy volunteers and patients with neurodegenerative disorders.

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