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本文引用的文献

1
Association of In Vivo [18F]AV-1451 Tau PET Imaging Results With Cortical Atrophy and Symptoms in Typical and Atypical Alzheimer Disease.体内[18F]AV-1451 tau PET 成像结果与典型和非典型阿尔茨海默病皮质萎缩和症状的关联。
JAMA Neurol. 2017 Apr 1;74(4):427-436. doi: 10.1001/jamaneurol.2016.5755.
2
In vivo Patterns of Tau Pathology, Amyloid-β Burden, and Neuronal Dysfunction in Clinical Variants of Alzheimer's Disease.阿尔茨海默病临床变异型中tau病理、β淀粉样蛋白负荷及神经元功能障碍的体内模式
J Alzheimers Dis. 2017;55(2):465-471. doi: 10.3233/JAD-160316.
3
An autoradiographic evaluation of AV-1451 Tau PET in dementia.AV-1451 tau PET 在痴呆症中的放射自显影评估。
Acta Neuropathol Commun. 2016 Jun 13;4(1):58. doi: 10.1186/s40478-016-0315-6.
4
Kinetics of the Tau PET Tracer 18F-AV-1451 (T807) in Subjects with Normal Cognitive Function, Mild Cognitive Impairment, and Alzheimer Disease.Tau正电子发射断层显像剂18F-AV-1451(T807)在认知功能正常、轻度认知障碍和阿尔茨海默病患者中的动力学研究
J Nucl Med. 2016 Oct;57(10):1535-1542. doi: 10.2967/jnumed.115.170027. Epub 2016 May 5.
5
Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer's disease.Tau正电子发射断层扫描(PET)模式反映了阿尔茨海默病的临床和神经解剖学变异性。
Brain. 2016 May;139(Pt 5):1551-67. doi: 10.1093/brain/aww027. Epub 2016 Mar 8.
6
Validating novel tau positron emission tomography tracer [F-18]-AV-1451 (T807) on postmortem brain tissue.在尸检脑组织上验证新型tau正电子发射断层显像示踪剂[F-18]-AV-1451(T807)
Ann Neurol. 2015 Nov;78(5):787-800. doi: 10.1002/ana.24517. Epub 2015 Sep 25.
7
The intersection of amyloid beta and tau at synapses in Alzheimer's disease.阿尔茨海默病中淀粉样β蛋白和tau 在突触处的交汇。
Neuron. 2014 May 21;82(4):756-71. doi: 10.1016/j.neuron.2014.05.004.
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Multi-atlas skull-stripping.多图谱颅骨剥离。
Acad Radiol. 2013 Dec;20(12):1566-76. doi: 10.1016/j.acra.2013.09.010.
9
A platform for discovery: The University of Pennsylvania Integrated Neurodegenerative Disease Biobank.一个发现平台:宾夕法尼亚大学综合神经退行性疾病生物样本库。
Alzheimers Dement. 2014 Jul;10(4):477-484.e1. doi: 10.1016/j.jalz.2013.06.003. Epub 2013 Aug 24.
10
Diverging patterns of amyloid deposition and hypometabolism in clinical variants of probable Alzheimer's disease.在可能的阿尔茨海默病的临床变异型中,淀粉样蛋白沉积和低代谢的模式存在差异。
Brain. 2013 Mar;136(Pt 3):844-58. doi: 10.1093/brain/aws327. Epub 2013 Jan 28.

F-Flortaucipir PET/MRI 与阿尔茨海默病非遗忘型和遗忘型变异的相关性。

F-Flortaucipir PET/MRI Correlations in Nonamnestic and Amnestic Variants of Alzheimer Disease.

机构信息

Department of Radiology, University of Pennsylvania, Philadelphia, Pennsylvania

Department of Radiology, University of Pennsylvania, Philadelphia, Pennsylvania.

出版信息

J Nucl Med. 2018 Feb;59(2):299-306. doi: 10.2967/jnumed.117.194282. Epub 2017 Jul 26.

DOI:10.2967/jnumed.117.194282
PMID:28747523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6348438/
Abstract

Nonamnestic Alzheimer disease (AD) variants, including posterior cortical atrophy and the logopenic variant of primary progressive aphasia, differ from amnestic AD in distributions of tau aggregates and neurodegeneration. We evaluated whether F-flortaucipir (also called F-AV-1451) PET, targeting tau aggregates, detects these differences, and we compared the results with MRI measures of gray matter (GM) atrophy. Five subjects with posterior cortical atrophy, 4 subjects with the logopenic variant of primary progressive aphasia, 6 age-matched patients with AD, and 6 control subjects underwent F-flortaucipir PET and MRI. SUV ratios and GM volumes were compared using regional and voxel-based methods. The subgroups showed the expected F-flortaucipir-binding patterns. Group effect sizes were generally stronger with F-flortaucipir PET than with MRI volumes. There were moderate-to-high correlations between regional GM atrophy and F-flortaucipir uptake. F-flortaucipir binding and GM atrophy correlated similarly to cognitive test performance. F-flortaucipir binding corresponds to the expected neurodegeneration patterns in nonamnestic AD, with potential for earlier detection of pathology than is possible with MRI atrophy measures.

摘要

非遗忘型阿尔茨海默病(AD)变体,包括后部皮质萎缩和原发性进行性失语的失语法变体,在tau 聚集物和神经退行性变的分布上与遗忘型 AD 不同。我们评估了靶向 tau 聚集物的 F-氟替卡培(也称为 F-AV-1451)PET 是否能检测到这些差异,并将结果与灰质(GM)萎缩的 MRI 测量值进行了比较。5 名后部皮质萎缩患者、4 名失语法原发性进行性失语患者、6 名年龄匹配的 AD 患者和 6 名对照受试者接受了 F-氟替卡培 PET 和 MRI 检查。使用基于区域和体素的方法比较了 SUV 比值和 GM 体积。亚组显示了预期的 F-氟替卡培结合模式。与 MRI 体积相比,F-氟替卡培 PET 的组效应大小通常更强。区域 GM 萎缩与 F-氟替卡培摄取之间存在中度至高相关性。F-氟替卡培结合与 GM 萎缩与认知测试表现的相关性相似。F-氟替卡培结合与非遗忘型 AD 中预期的神经退行性变模式相对应,与 MRI 萎缩测量相比,有可能更早地检测到病理。