Disease-related patterns of in vivo pathology in Corticobasal syndrome.

Disease-related patterns of in vivo pathology in Corticobasal syndrome.
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DOI:
10.1007/s00259-018-4104-2
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发表时间:
2018-12
影响因子:
9.1
通讯作者:
Alzheimer’s Disease Neuroimaging Initiative
Alzheimer’s Disease Neuroimaging Initiative
中科院分区:
医学1区
文献类型:
--
作者:
Niccolini F;Wilson H;Hirschbichler S;Yousaf T;Pagano G;Whittington A;Caminiti SP;Erro R;Holton JL;Jaunmuktane Z;Esposito M;Martino D;Abdul A;Passchier J;Rabiner EA;Gunn RN;Bhatia KP;Politis M;Alzheimer’s Disease Neuroimaging Initiative

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评估11例皮质基底综合征(CBS)患者体内病理的疾病相关模式,与20例健康对照和33例阿尔茨海默病引起的轻度认知障碍(MCI)患者进行比较。我们用[18F]AV1451 PET评估tau聚集物,用[18F]AV45 PET评估淀粉样蛋白-β沉积,并用MRI评估体积微结构变化。我们验证了[18F]AV1451标准化摄取值比(SUVRs)与动脉代谢物输入功能的对比,发现SUVRs和动脉源性分布体积比(dvr)提供了[18F]AV1451结合的同样可靠的测量。与健康对照组相比,CBS患者患半球顶叶(P < 0.05)和额叶(P < 0.05)皮质的AV1451 SUVRs [18F]增加,与MCI患者相比,患半球中央前回(P = 0.008)和中央后回(P = 0.034)的AV1451 SUVRs增加。我们的数据在一名接受脑活检的CBS患者的组织病理学水平上得到了证实,该患者在顶叶皮层共定位中显示出稀疏的tau病理学,并伴有AV1451信号升高[18F]。CBS患者的皮质和皮质下[18F]AV45摄取处于正常水平。在最受影响的顶叶和额叶皮层,我们发现与健康对照组和MCI患者相比,CBS患者的灰质减少(P < 0.05),平均扩散率增加(P < 0.05),分数各向异性降低(P < 0.05)。CBS患者中枢前回灰质丢失和白质改变与更严重的运动症状相关。我们的研究结果表明,在没有淀粉样蛋白-β的情况下,体内tau和微观结构病理的疾病相关模式将CBS与未受影响的个体和MCI患者区分开来。本文的在线版本(10.1007/s00259-018- 4102 -2)包含补充资料,仅供授权用户使用。
To assess disease-related patterns of in vivo pathology in 11 patients with Corticobasal Syndrome (CBS) compared to 20 healthy controls and 33 mild cognitive impairment (MCI) patients due to Alzheimer’s disease. We assessed tau aggregates with [18F]AV1451 PET, amyloid-β depositions with [18F]AV45 PET, and volumetric microstructural changes with MRI. We validated for [18F]AV1451 standardised uptake value ratio (SUVRs) against input functions from arterial metabolites and found that SUVRs and arterial-derived distribution volume ratio (DVRs) provide equally robust measures of [18F]AV1451 binding. CBS patients showed increases in [18F]AV1451 SUVRs in parietal (P < 0.05) and frontal (P < 0.05) cortices in the affected hemisphere compared to healthy controls and in precentral (P = 0.008) and postcentral (P = 0.034) gyrus in the affected hemisphere compared to MCI patients. Our data were confirmed at the histopathological level in one CBS patient who underwent brain biopsy and showed sparse tau pathology in the parietal cortex co-localizing with increased [18F]AV1451 signal. Cortical and subcortical [18F]AV45 uptake was within normal levels in CBS patients. In parietal and frontal cortices of the most affected hemisphere we found also grey matter loss (P < 0.05), increased mean diffusivity (P < 0.05) and decreased fractional anisotropy (P < 0.05) in CBS patients compared to healthy controls and MCI patients. Grey matter loss and white matter changes in the precentral gyrus of CBS patients were associated with worse motor symptoms. Our findings demonstrate disease-related patterns of in vivo tau and microstructural pathology in the absence of amyloid-β, which distinguish CBS from non-affected individuals and MCI patients. The online version of this article (10.1007/s00259-018-4104-2) contains supplementary material, which is available to authorized users.
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