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18F-AV-1451 positron emission tomography in neuropathological substrates of corticobasal syndrome.

18F-AV-1451皮质基底综合征神经病理基质的正电子发射断层扫描。

  • 影响因子:0
  • DOI:10.1093/brain/awaa383
  • 作者列表:"Goodheart AE","Locascio JJ","Samore WR","Collins JA","Brickhouse M","Schultz A","Touroutoglou A","Johnson KA","Frosch MP","Growdon JH","Dickerson BC","Gomperts SN
  • 发表时间:2021-02-12
Abstract

:Multiple neuropathological processes can manifest in life as a corticobasal syndrome. We sought to relate retention of the tau-PET tracer 18F-AV-1451 and structural magnetic resonance measures of regional atrophy to clinical features in clinically diagnosed and neuropathologically confirmed cases of corticobasal syndrome and to determine whether these vary with the underlying neuropathological changes. In this observational, cross-sectional study, 11 subjects (eight female and three male, median age 72 years) with corticobasal syndrome underwent structural MRI, tau-PET with 18F-AV-1451, amyloid-PET with 11C-Pittsburgh compound B, detailed clinical examinations and neuropsychological testing. Of the 11, three had evidence of high amyloid burden consistent with Alzheimer's disease while eight did not. Neuropathological evaluations were acquired in six cases. Mixed effects general linear models were used to compare 18F-AV-1451 retention and atrophy in amyloid-negative corticobasal syndrome cases to 32 age-matched healthy control subjects and to relate cortical and subcortical 18F-AV-1451 retention and atrophy to clinical features. Subjects without amyloid, including three with pathologically confirmed corticobasal degeneration, showed greater regional 18F-AV-1451 retention and associated regional atrophy in areas commonly associated with corticobasal degeneration pathology than healthy control subjects [retention was higher compared to healthy controls (P = 0.0011), driven especially by the precentral gyrus (P = 0.011) and pallidum (P < 0.0001), and greater atrophy was seen in subjects compared to control subjects (P = 0.0004)]. Both 18F-AV-1451 retention and atrophy were greater in the clinically more affected hemisphere [on average, retention was 0.173 standardized uptake value ratio units higher on the more affected side (95% confidence interval, CI 0.11-0.24, P < 0.0001), and volume was 0.719 lower on the more affected side (95% CI 0.35-1.08, P = 0.0001)]. 18F-AV-1451 retention was greater in subcortical than in cortical regions, P < 0.0001. In contrast to these findings, subjects with amyloid-positive corticobasal syndrome, including two neuropathologically confirmed cases of Alzheimer's disease, demonstrated greater and more widespread 18F-AV-1451 retention and regional atrophy than observed in the amyloid-negative cases. There was thalamic 18F-AV-1451 retention but minimal cortical and basal ganglia uptake in a single corticobasal syndrome subject without neuropathological evidence of tau pathology, likely representing non-specific signal. Asymmetric cortical and basal ganglia 18F-AV-1451 retention consonant with the clinical manifestations characterize corticobasal syndrome due to corticobasal degeneration, whereas the cortical retention in cases associated with Alzheimer's disease is greater and more diffuse.

摘要

: 多种神经病理过程可在生活中表现为皮质基底综合征。我们试图将tau-PET示踪剂18F-AV-1451的保留和区域萎缩的结构磁共振测量与皮质基底综合征临床诊断和神经病理学确诊病例的临床特征联系起来,并确定这些特征是否随潜在的神经病理学变化而变化。在这项观察性横断面研究中,11名皮质基底综合征受试者 (8名女性和3名男性,中位年龄72岁) 接受了结构MRI、tau-PET (18F-AV-1451) 、淀粉样蛋白-PET (11C-Pittsburgh compound B) 、详细的临床检查和神经心理测试。在这11人中,3人有与阿尔茨海默病一致的高淀粉样蛋白负担的证据,而8人没有。6例获得神经病理学评价。混合效应一般线性模型用于比较淀粉样蛋白阴性皮质基底综合征病例中的18F-AV-1451保留和萎缩与32名年龄匹配的健康对照受试者,并将皮质和皮质下的18F-AV-1451保留和萎缩与临床特征联系起来。没有淀粉样蛋白的受试者,包括三个病理证实为皮质变性的受试者,在通常与皮质变性病理相关的区域显示出比健康对照受试者更大的区域18F-AV-1451保留和相关的区域萎缩 [保留高于健康对照 (p   =   0.0011),特别是由中央前回驱动 (p   =   0.011) 和苍白球 (p <0.0001),并且与对照受试者相比,在受试者中观察到更大的萎缩 (p   =   0.0004)]。18F-AV-1451保留和萎缩在临床上受影响较大的半球中更大 [平均而言,受影响较大的一侧保留为0.173标准化摄取值比单位高 (95% 置信区间,CI 0.11-0.24,p <0.0001),患侧的体积降低了0.719 (95% CI 0.35-1.08,p = 0.0001)。18F-AV-1451在皮质下的保留大于皮质区,p <0.0001。与这些发现相反,患有淀粉样蛋白阳性皮质基底综合征 (包括两种阿尔茨海默病的神经病理学确诊病例) 的受试者表现出比在淀粉样蛋白阴性病例中观察到的更大且更广泛的18F-AV-1451保留和区域萎缩。在没有tau病理学神经病理学证据的单个皮质基底综合征受试者中存在丘脑18F-AV-1451保留,但皮质和基底神经节摄取很少,可能代表非特异性信号。不对称的皮质和基底神经节18F-AV-1451与临床表现一致的保留是由于皮质退化引起的皮质基底综合征的特征,而与阿尔茨海默病相关的病例的皮质保留更大且更弥漫。

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