小胶质细胞
病理
帕金森病
医学
基底神经节
壳核
正电子发射断层摄影术
神经炎症
体内
脑干
结合势
神经科学
中枢神经系统
内科学
疾病
心理学
生物
核医学
炎症
生物技术
作者
Alexander Gerhard,Nicola Pavese,Gary Hotton,Federico Turkheimer,Meltem Es,Alexander Hammers,Karla Eggert,Wolfgang H. Oertel,Richard B. Bánati,David J. Brooks
标识
DOI:10.1016/j.nbd.2005.08.002
摘要
Idiopathic Parkinson's disease (PD) is a neurodegenerative disorder associated with akinesia, tremor and rigidity. While the characteristic Lewy body pathology targets pigmented and other brainstem nuclei at post-mortem, activated microglia are found in both subcortical and cortical areas. [11C](R)-PK11195 is a positron emission tomography (PET) marker of peripheral benzodiazepine sites (PBBS), which are selectively expressed by activated microglia. We examined 18 PD patients clinically and with [11C](R)-PK11195 and [18F]-dopa PET. Compared to 11 normal controls, the PD patients showed significantly increased mean levels of [11C](R)-PK11195 binding in the pons, basal ganglia and frontal and temporal cortical regions. Eight PD patients were examined longitudinally, and their [11C](R)-PK11195 signal remained stable over 2 years. Levels of microglial activation did not correlate with clinical severity or putamen [18F]-dopa uptake. Our in vivo findings confirm that widespread microglial activation is associated with the pathological process in PD. The absence of significant longitudinal changes suggests that microglia are activated early in the disease process, and levels then remain relatively static, possibly driving the disease via cytokine release.
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