RT Journal Article
SR Electronic
T1 PET of Glial Metabolism Using 2-<sup>18</sup>F-Fluoroacetate
JF Journal of Nuclear Medicine
JO J Nucl Med
FD Society of Nuclear Medicine
SP 982
OP 990
DO 10.2967/jnumed.108.057356
VO 50
IS 6
A1 Marik, Jan
A1 Ogasawara, Annie
A1 Martin-McNulty, Baby
A1 Ross, Jed
A1 Flores, Judith E.
A1 Gill, Herman S.
A1 Tinianow, Jeff N.
A1 Vanderbilt, Alexander N.
A1 Nishimura, Merry
A1 Peale, Franklin
A1 Pastuskovas, Cinthia
A1 Greve, Joan M.
A1 van Bruggen, Nicholas
A1 Williams, Simon P.
YR 2009
UL http://jnm.snmjournals.org/content/50/6/982.abstract
AB 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.