Department of Nuclear Medicine and Molecular Imaging, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands Department of Neuroscience, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands Center of Nuclear Medicine, University of Sao Paulo Medical School, University of Sao Paulo, Sao Paulo, Brazil.
TNO, Zeist, The Netherlands; and.
J Nucl Med. 2014 Aug;55(8):1330-5. doi: 10.2967/jnumed.114.137216. Epub 2014 Jun 9.
The experimental autoimmune encephalomyelitis model is a model of multiple sclerosis that closely mimics the disease characteristics in humans. The main hallmarks of multiple sclerosis are neuroinflammation (microglia activation, monocyte invasion, and T-cell infiltration) and demyelination. PET imaging may be a useful noninvasive technique for monitoring disease progression and drug treatment efficacy in vivo.
Experimental autoimmune encephalomyelitis was induced by myelin-oligodendrocyte glycoprotein immunization in female Dark Agouti rats. Experimental autoimmune encephalomyelitis rats were imaged at baseline and at days 6, 11, 15, and 19 after immunization to monitor monocyte and microglia activation ((11)C-PK11195) and demyelination ((11)C-MeDAS) during normal disease progression and during treatment with dexamethasone.
(11)C-PK11195 PET detected activation of microglia and monocytes in the brain stem and spinal cord during disease progression. The uptake of (11)C-PK11195 was elevated in dexamethasone-treated animals that had shown mild clinical symptoms that had resolved at the time of imaging. Demyelination was not detected by (11)C-MeDAS PET, probably because of the small size of the lesions (average, 0.13 mm).
PET imaging of neuroinflammation can be used to monitor disease progression and the consequences of treatment in the experimental autoimmune encephalomyelitis rat model. PET imaging was more sensitive than clinical symptoms for detecting inflammatory changes in the central nervous system.
实验性自身免疫性脑脊髓炎模型是多发性硬化症的一种模型，它非常类似于人类的疾病特征。多发性硬化症的主要特征是神经炎症（小胶质细胞激活、单核细胞浸润和 T 细胞浸润）和脱髓鞘。PET 成像可能是一种有用的非侵入性技术，可用于监测疾病进展和体内药物治疗效果。
通过髓鞘少突胶质细胞糖蛋白免疫在雌性 Dark Agouti 大鼠中诱导实验性自身免疫性脑脊髓炎。在免疫后第 6、11、15 和 19 天对实验性自身免疫性脑脊髓炎大鼠进行成像，以监测单核细胞和小胶质细胞激活（11C-PK11195）和脱髓鞘（11C-MeDAS）在正常疾病进展期间以及在使用地塞米松治疗期间。
（11C-PK11195 PET 在疾病进展过程中检测到脑脑干和脊髓中小胶质细胞和单核细胞的激活。在已经出现轻度临床症状但在成像时已经缓解的地塞米松治疗动物中，（11C-PK11195 的摄取增加。（11C-MeDAS PET 未检测到脱髓鞘，可能是因为病变较小（平均为 0.13 毫米）。
神经炎症的 PET 成像可用于监测实验性自身免疫性脑脊髓炎大鼠模型中的疾病进展和治疗后果。PET 成像比临床症状更能检测中枢神经系统中的炎症变化。
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