Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
J Neuroinflammation. 2018 Dec 19;15(1):346. doi: 10.1186/s12974-018-1381-4.
The pathophysiology of post-treatment Lyme disease syndrome (PTLDS) may be linked to overactive immunity including aberrant activity of the brain's resident immune cells, microglia. Here we used [C]DPA-713 and positron emission tomography to quantify the 18 kDa translocator protein, a marker of activated microglia or reactive astrocytes, in the brains of patients with post-treatment Lyme disease symptoms of any duration compared to healthy controls. Genotyping for the TSPO rs6971 polymorphism was completed, and individuals with the rare, low affinity binding genotype were excluded. Data from eight brain regions demonstrated higher [C]DPA-713 binding in 12 patients relative to 19 controls. [C]DPA-713 PET is a promising tool to study cerebral glial activation in PTLDS and its link to cognitive symptoms.
治疗后莱姆病综合征 (PTLDS) 的病理生理学可能与过度活跃的免疫有关，包括大脑常驻免疫细胞——小胶质细胞的异常活动。在这里，我们使用 [C]DPA-713 和正电子发射断层扫描来定量分析治疗后莱姆病症状持续时间任何患者的大脑中 18kDa 转位蛋白（一种激活的小胶质细胞或反应性星形胶质细胞的标志物），并与健康对照组进行比较。完成了 TSPO rs6971 多态性的基因分型，并排除了具有罕见、低亲和力结合基因型的个体。来自八个脑区的数据表明，12 名患者的 [C]DPA-713 结合高于 19 名对照者。[C]DPA-713 PET 是一种有前途的工具，可用于研究 PTLDS 中的脑胶质细胞激活及其与认知症状的关系。
