Tai Y F, Ahsan R L, de Yébenes J G, Pavese N, Brooks D J, Piccini P
MRC Clinical Sciences Centre and Division of Neurosciences, Hammersmith Hospital, Imperial College London, United Kingdom.
J Neural Transm (Vienna). 2007 Mar;114(3):337-40. doi: 10.1007/s00702-006-0536-0. Epub 2006 Aug 8.
We analyzed (18)F-dopa PET data from 11 members of kindreds with familial progressive supranuclear palsy (PSP) to characterize their cerebral dopaminergic dysfunction. Three clinically-affected PSP patients showed reduced (18)F-dopa uptake in the striatum, orbitofrontal cortex and amygdala. One asymptomatic subject exhibited progressive putamen dopaminergic dysfunction. 60% of subjects with abnormal (18)F-dopa scans developed PSP subsequently. This is the first in vivo documentation of cortical dopaminergic deficiency in PSP. Reduced striatal (18)F-dopa uptake in susceptible relatives may predict later clinical disease.
我们分析了来自11个家族性进行性核上性麻痹（PSP）家族成员的（18）F-多巴PET数据，以表征他们的脑多巴胺能功能障碍。三名临床确诊的PSP患者在纹状体、眶额皮质和杏仁核中显示出（18）F-多巴摄取减少。一名无症状受试者表现出进行性壳核多巴胺能功能障碍。（18）F-多巴扫描异常的受试者中有60%随后发展为PSP。这是PSP中皮质多巴胺能缺乏的首次体内记录。易感亲属纹状体（18）F-多巴摄取减少可能预示着以后的临床疾病。
