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PET of Glial Metabolism Using 2-¹⁸F-Fluoroacetate

¹ Biomedical Imaging, Genentech Inc., South San Francisco, California; ² Department of Tumor Biology and Angiogenesis, Genentech Inc., South San Francisco, California; ³ Research Pathology, Genentech Inc., South San Francisco, California; and ⁴ Early Development PKPD, Genentech Inc., South San Francisco, California

Correspondence: For correspondence or reprints contact: Jan Marik, Biomedical Imaging, Genentech Inc., One DNA Way, Mailstop 228, South San Francisco, CA 94080. E-mail: marik.jan{at}gene.com

Imaging of the glial activation that occurs in response to central nervous system trauma and inflammation could become a powerful technique for the assessment of several neuropathologies. The selective uptake and metabolism of 2-¹⁸F-fluoroacetate (¹⁸F-FAC) in glia may represent an attractive strategy for imaging glial metabolism. Methods: We have evaluated the use of ¹⁸F-FAC as a specific PET tracer of glial cell metabolism in rodent models of glioblastoma, stroke, and ischemia–hypoxia. Results: Enhanced uptake of ¹⁸F-FAC was observed (6.98 ± 0.43 percentage injected dose per gram [%ID/g]; tumor-to-normal ratio, 1.40) in orthotopic U87 xenografts, compared with healthy brain tissue. The lesion extent determined by ¹⁸F-FAC PET correlated with that determined by MRI (R² = 0.934, P = 0.007). After transient middle cerebral artery occlusion in the rat brain, elevated uptake of ¹⁸F-FAC (1.00 ± 0.03 %ID/g; lesion-to-normal ratio, 1.90) depicted the ischemic territory and correlated with infarct volumes as determined by 2,3,5-triphenyltetrazolium chloride staining (R² = 0.692, P = 0.010) and with the presence of activated astrocytes detected by anti–glial fibrillary acidic protein. Ischemia–hypoxia, induced by permanent ligation of the common carotid artery with transient hypoxia, resulted in persistent elevation of ¹⁸F-FAC uptake within 30 min of the induction of hypoxia. Conclusion: Our data support the further evaluation of ¹⁸F-FAC PET for the assessment of glial cell metabolism associated with neuroinflammation.

Key Words: PET • glial metabolism • 2-¹⁸F-fluoroacetate • ischemia-hypoxia • stroke • glioblastoma

COPYRIGHT © 2009 by the Society of Nuclear Medicine, Inc.

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