PET of Glial Metabolism Using 2-18F-Fluoroacetate

被引:37
|
作者
Marik, Jan [1 ]
Ogasawara, Annie [1 ]
Martin-McNulty, Baby [1 ]
Ross, Jed [1 ]
Flores, Judith E. [1 ]
Gill, Herman S. [1 ]
Tinianow, Jeff N. [1 ]
Vanderbilt, Alexander N. [1 ]
Nishimura, Merry [2 ]
Peale, Franklin [3 ]
Pastuskovas, Cinthia [4 ]
Greve, Joan M. [1 ]
van Bruggen, Nicholas [1 ]
Williams, Simon P. [1 ]
机构
[1] Genentech Inc, Biomed Imaging, San Francisco, CA 94080 USA
[2] Genentech Inc, Dept Tumor Biol & Angiogenesis, San Francisco, CA 94080 USA
[3] Genentech Inc, Res Pathol, San Francisco, CA 94080 USA
[4] Genentech Inc, Early Dev PKPD, San Francisco, CA 94080 USA
关键词
PET; glial metabolism; 2-F-18-fluoroacetate; ischemia-hypoxia; stroke; glioblastoma; CEREBRAL-ARTERY OCCLUSION; RADIATION-DOSE ESCALATION; GLIOBLASTOMA-MULTIFORME; CRYSTAL-STRUCTURE; BRAIN-TUMORS; F-18-FDG PET; ISCHEMIA; FLUOROACETATE; RAT; ACETATE;
D O I
10.2967/jnumed.108.057356
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
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-F-18-fluoroacetate (F-18-FAC) in glia may represent an attractive strategy for imaging glial metabolism. Methods: We have evaluated the use of F-18-FAC as a specific PET tracer of glial cell metabolism in rodent models of glioblastoma, stroke, and ischemia-hypoxia. Results: Enhanced uptake of F-18-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 F-18-FAC PET correlated with that determined by MRI (R-2 = 0.934, P = 0.007). After transient middle cerebral artery occlusion in the rat brain, elevated uptake of F-18-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 (R-2 = 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 F-18-FAC uptake within 30 min of the induction of hypoxia. Conclusion: Our data support the further evaluation of F-18-FAC PET for the assessment of glial cell metabolism associated with neuroinflammation.
引用
收藏
页码:982 / 990
页数:9
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