Abstract:
:Reduced nigrostriatal uptake on N-(3-fluoropropyl)-2β-carbomethoxy-3β-(4-[123I]iodophenyl) nortropane (123I-FP-CIT) SPECT reflects dopamine dysfunction, while other imaging markers could be complementary when used together. We assessed how well 123I-FP-CIT SPECT differentiates dementia with Lewy bodies (DLBs) from Alzheimer's disease dementia (ADem) and whether multimodal imaging provides additional value. 123I-FP-CIT SPECT, magnetic resonance imaging, [18F]2-fluoro-deoxy-D-glucose-positron emission tomography (PET), and 11C-Pittsburgh compound B (PiB)-PET were assessed in 35 participants with DLBs and 14 participants with ADem (autopsy confirmation in 9 DLBs and 4 ADem). Nigrostriatal dopamine transporter uptake was evaluated with 123I-FP-CIT SPECT using DaTQUANT software. Hippocampal volume was calculated with magnetic resonance imaging, cingulate island sign ratio with FDG-PET, and global cortical PiB retention with PiB-PET. The DaTQUANT z-scores of the putamen showed the highest c-statistic of 0.916 in differentiating DLBs from ADem among the analyzed imaging biomarkers. Adding another imaging modality to 123I-FP-CIT SPECT had c-statistics ranging from 0.968 to 0.975, and 123I-FP-CIT SPECT in combination with 2 other imaging modalities presented c-statistics ranging from 0.987 to 0.996. These findings suggest that multimodal imaging with 123I-FP-CIT SPECT aids in differentiating DLBs and ADem and in detecting comorbid Lewy-related and Alzheimer's disease pathology in patients with DLBs and ADem.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Miyagawa T,Przybelski SA,Maltais D,Min HK,Jordan L,Lesnick TG,Chen Q,Graff-Radford J,Jones D,Savica R,Knopman D,Petersen R,Kremers WK,Forsberg LK,Fields JA,Ferman TJ,Allen L,Parisi J,Reichard RR,Murray M,Dickson Ddoi
10.1016/j.neurobiolaging.2020.12.009subject
Has Abstractpub_date
2020-12-15 00:00:00pages
11-18eissn
0197-4580issn
1558-1497pii
S0197-4580(20)30418-8journal_volume
99pub_type
杂志文章abstract::Linkage data in Alzheimer's disease have not firmly established a genetic locus on chromosome 21 in early onset disease families. There is little or no support for a chromosome 21 locus in late onset families. Differences in the selection of families and the analysis of data accounts for the differences in interpretat...
journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2014.07.032
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2009.11.006
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/0197-4580(90)90044-z
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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