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 Laere^3,4, Michel Koole⁴, Wim Vandenberghe⁵, Eugenii Rabiner^1,6, 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

Synopsis

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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