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Multimodality imaging characteristics of dementia with Lewy bodies.路易体痴呆的多模态影像学特征。
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2
Regional glucose metabolic reduction in dementia with Lewy bodies is independent of amyloid deposition.路易体痴呆患者局部葡萄糖代谢降低与淀粉样蛋白沉积无关。
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AV-1451 tau and β-amyloid positron emission tomography imaging in dementia with Lewy bodies.AV-1451 tau与β-淀粉样蛋白正电子发射断层扫描成像在路易体痴呆中的应用
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Amyloid and glucose imaging in dementia with Lewy bodies and multiple systems atrophy.路易体痴呆和多系统萎缩的淀粉样蛋白和葡萄糖成像。
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Syndrome-specific patterns of regional cerebral glucose metabolism in posterior cortical atrophy in comparison to dementia with Lewy bodies and Alzheimer's disease--a [F-18]-FDG pet study.与路易体痴呆和阿尔茨海默病相比,后皮质萎缩中脑葡萄糖代谢区域的综合征特异性模式——一项[F-18] - FDG PET研究。
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Early differential diagnosis between Alzheimer's disease and dementia with Lewy bodies: Comparison between (18)F-FDG PET and (123)I-IMP SPECT.阿尔茨海默病与路易体痴呆的早期鉴别诊断:(18)F-FDG PET与(123)I-IMP SPECT的比较
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Distinguishing between dementia with Lewy bodies and Alzheimer's disease using metabolic patterns.利用代谢模式区分路易体痴呆和阿尔茨海默病。
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β-Amyloid in Lewy body disease is related to Alzheimer's disease-like atrophy.路易体病中的β-淀粉样蛋白与阿尔茨海默病样萎缩有关。
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Two distinct pathological substrates associated with MMSE-pentagons item deficit in DLB and AD.两种不同的病理基础与 DLB 和 AD 患者 MMSE 五边形项目缺陷相关。
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Correlating hippocampal and amygdala volumes with neuropathological burden in Down syndrome and Alzheimer's disease and related neurodegenerative pathologies using 7T postmortem MRI.利用7T尸检MRI将唐氏综合征、阿尔茨海默病及相关神经退行性病变中的海马体和杏仁核体积与神经病理学负担相关联。
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Right anterior insula ASL hypoperfusion as a diagnostic biomarker of prodromal and mild dementia with Lewy bodies: preliminary evidence using a Bayesian approach.右前岛叶动脉自旋标记灌注减低作为前驱期和轻度路易体痴呆的诊断生物标志物:基于贝叶斯方法的初步证据
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[Dementia with Lewy bodies: old and new knowledge - Part 1: clinical aspects and diagnostics].[路易体痴呆:新旧知识 - 第1部分:临床方面与诊断]
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Identifying individuals with non-Alzheimer's disease co-pathologies: A precision medicine approach to clinical trials in sporadic Alzheimer's disease.识别伴有非阿尔茨海默病共病的个体:在散发性阿尔茨海默病临床试验中的精准医学方法。
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The Mechanisms of the Roles of α-Synuclein, Amyloid-β, and Tau Protein in the Lewy Body Diseases: Pathogenesis, Early Detection, and Therapeutics.α-突触核蛋白、淀粉样β和tau 蛋白在路易体疾病中的作用机制:发病机制、早期检测和治疗。
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本文引用的文献

1
PET imaging of brain amyloid in dementia: a review.正电子发射断层扫描(PET)脑淀粉样蛋白成像在痴呆症中的应用:综述。
Int J Geriatr Psychiatry. 2011 Oct;26(10):991-9. doi: 10.1002/gps.2640. Epub 2010 Dec 28.
2
High resolution imaging of the medial temporal lobe in Alzheimer's disease and dementia with Lewy bodies.阿尔茨海默病和路易体痴呆症内侧颞叶的高分辨率成像。
J Alzheimers Dis. 2010;21(4):1129-40. doi: 10.3233/jad-2010-100138.
3
Neuropathological correlates of volumetric MRI in autopsy-confirmed Lewy body dementia.尸检确诊的路易体痴呆症患者的磁共振体积成像的神经病理学相关性。
Neurobiol Aging. 2012 Jul;33(7):1228-36. doi: 10.1016/j.neurobiolaging.2010.12.015. Epub 2011 Feb 24.
4
In vivo fibrillar beta-amyloid detected using [11C]PiB positron emission tomography and neuropathologic assessment in older adults.在老年人中使用[11C]匹兹堡化合物B正电子发射断层扫描检测体内纤维状β-淀粉样蛋白并进行神经病理学评估。
Arch Neurol. 2011 Feb;68(2):232-40. doi: 10.1001/archneurol.2010.357.
5
Antemortem differential diagnosis of dementia pathology using structural MRI: Differential-STAND.使用结构 MRI 对痴呆病理进行生前鉴别诊断:Differential-STAND。
Neuroimage. 2011 Mar 15;55(2):522-31. doi: 10.1016/j.neuroimage.2010.12.073. Epub 2010 Dec 31.
6
Improved visual hallucination by donepezil and occipital glucose metabolism in dementia with Lewy bodies: the Osaki-Tajiri project.多奈哌齐改善路易体痴呆患者的视幻觉和枕叶葡萄糖代谢:大崎-田尻计划。
Eur Neurol. 2010;64(6):337-44. doi: 10.1159/000322121. Epub 2010 Nov 13.
7
Antemortem amyloid imaging and β-amyloid pathology in a case with dementia with Lewy bodies.路易体痴呆症一例的生前淀粉样蛋白成像与β-淀粉样蛋白病理学。
Neurobiol Aging. 2012 May;33(5):878-85. doi: 10.1016/j.neurobiolaging.2010.08.007. Epub 2010 Oct 18.
8
Striatal Aβ peptide deposition mirrors dementia and differentiates DLB and PDD from other parkinsonian syndromes.纹状体 Aβ 肽沉积反映了痴呆,并将 DLB 和 PDD 与其他帕金森综合征区分开来。
Neurobiol Dis. 2011 Feb;41(2):377-84. doi: 10.1016/j.nbd.2010.10.005. Epub 2010 Oct 14.
9
Amyloid imaging of Lewy body-associated disorders.路易体相关疾病的淀粉样蛋白成像。
Mov Disord. 2010 Nov 15;25(15):2516-23. doi: 10.1002/mds.23393.
10
Distribution of cerebral amyloid deposition and its relevance to clinical phenotype in Lewy body dementia.路易体痴呆症中脑淀粉样蛋白沉积的分布及其与临床表型的相关性。
Neurosci Lett. 2010 Dec 3;486(1):19-23. doi: 10.1016/j.neulet.2010.09.036. Epub 2010 Sep 17.

路易体痴呆的多模态影像学特征。

Multimodality imaging characteristics of dementia with Lewy bodies.

机构信息

Department of Radiology, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

Neurobiol Aging. 2012 Sep;33(9):2091-105. doi: 10.1016/j.neurobiolaging.2011.09.024. Epub 2011 Oct 21.

DOI:10.1016/j.neurobiolaging.2011.09.024
PMID:22018896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3288845/
Abstract

Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia after Alzheimer's disease (AD). Our objective was to determine whether the (11)C-Pittsburgh Compound-B (PiB) retention and regional hypometabolism on positron emission tomography (PET) and regional cortical atrophy on magnetic resonance imaging (MRI) are complementary in characterizing patients with DLB and differentiating them from AD. We studied age-, gender-, and education-matched patients with a clinical diagnosis of DLB (n = 21), AD (n = 21), and cognitively normal subjects (n = 42). Hippocampal atrophy, global cortical PiB retention and occipital lobe metabolism in combination distinguished DLB from AD better than any of the measurements alone (area under the receiver operating characteristic = 0.98). Five of the DLB and AD patients who underwent autopsy were distinguished through multimodality imaging. These data demonstrate that magnetic resonance imaging and PiB positron emission tomography contribute to characterizing the distinct pathological mechanisms in patients with AD compared with DLB. Occipital and posterior parietotemporal lobe hypometabolism is a distinguishing feature of DLB and this regional hypometabolic pattern is independent of the amyloid pathology.

摘要

路易体痴呆(DLB)是仅次于阿尔茨海默病(AD)的第二大常见神经退行性痴呆病因。我们的目的是确定正电子发射断层扫描(PET)上的(11)C-匹兹堡化合物-B(PiB)保留和区域性低代谢以及磁共振成像(MRI)上的区域性皮质萎缩是否可以互补,以对 DLB 患者进行特征描述并将其与 AD 区分开来。我们研究了年龄、性别和教育相匹配的具有临床诊断的 DLB(n = 21)、AD(n = 21)和认知正常的受试者(n = 42)。海马萎缩、全局皮质 PiB 保留和枕叶代谢结合起来,比任何单独的测量都能更好地区分 DLB 和 AD(接受者操作特征曲线下面积= 0.98)。5 名接受过尸检的 DLB 和 AD 患者通过多模态成像得以区分。这些数据表明,磁共振成像和 PiB 正电子发射断层扫描有助于对 AD 患者与 DLB 患者的不同病理机制进行特征描述。枕叶和后顶叶皮质代谢低下是 DLB 的一个显著特征,这种区域性代谢低下模式与淀粉样蛋白病理学无关。