PET of Glial Metabolism Using 2-18F-Fluoroacetate

PET of Glial Metabolism Using 2-18F-Fluoroacetate
复制标题

DOI:
10.2967/jnumed.108.057356
复制
发表时间:
2009-06-01
影响因子:
9.3
通讯作者:
Williams, Simon P.
Williams, Simon P.
中科院分区:
医学1区
文献类型:
--
作者:
Marik, Jan;Ogasawara, Annie;Williams, Simon P.

文献摘要

被引文献

相似文献

中枢神经系统损伤和炎症反应中发生的神经胶质激活的成像可能成为评估几种神经病理学的有力技术。2- f -18-氟乙酸酯(F-18-FAC)在胶质细胞中的选择性摄取和代谢可能是一种有吸引力的胶质代谢成像策略。方法:我们评估了F-18-FAC作为胶质母细胞瘤、中风和缺血-缺氧啮齿动物模型中胶质细胞代谢的特异性PET示踪剂的使用。结果:与健康脑组织相比,原位U87异种移植物对F-18-FAC的摄取增强(6.98 +/- 0.43注射剂量/克[%ID/g];瘤正常比为1.40)。F-18-FAC PET检查与MRI检查的病变程度相关(R-2 = 0.934, P = 0.007)。大鼠脑短暂性大脑中动脉闭塞后,F-18-FAC摄取升高(1.00 +/- 0.03% ID/g;病变与正常比值1.90)描绘了缺血区域,并与2,3,5-三苯四氮唑氯染色测定的梗死体积相关(R-2 = 0.692, P = 0.010),与抗胶质纤维酸性蛋白检测的活化星形胶质细胞存在相关。永久性结扎颈总动脉并短暂性缺氧导致缺血-缺氧,导致缺氧诱导后30分钟内F-18-FAC摄取持续升高。结论:我们的数据支持进一步评估F-18-FAC PET对神经炎症相关胶质细胞代谢的评估。
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.