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Distinguishing between dementia with Lewy bodies and Alzheimer's disease using metabolic patterns

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dc.contributor.author손영호-
dc.contributor.author예병석-
dc.contributor.author유한수-
dc.contributor.author윤미진-
dc.contributor.author이양현-
dc.contributor.author이필휴-
dc.contributor.author정석종-
dc.date.accessioned2020-04-13T17:04:19Z-
dc.date.available2020-04-13T17:04:19Z-
dc.date.issued2020-
dc.identifier.issn0197-4580-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/175632-
dc.description.abstractAlzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the 2 most common causes of dementia. We compared the regional metabolism on 18F-fluorodeoxyglucose positron emission tomography (PET) among 21 control subjects and cognitively impaired patients due to DLB (N = 63) and AD (N = 38). All participants underwent 18F-Florbetaben (FBB) PET, and all DLB patients had abnormality on dopamine transporter PET. Both the FBB-positive DLB (N = 38) and FBB-negative DLB (N = 25) groups had increased metabolism in the bilateral central cerebellum, posterior putamen, and somatomotor cortices compared with the control and AD groups. Compared with the control group, the DLB and AD groups commonly exhibited hypometabolism in the bilateral lateral temporal, temporo-parietal junction, posterior cingulate, and precuneus cortices. Both DLB groups had additional hypometabolism in the bilateral thalami and dorsolateral prefrontal cortices, whereas the AD group did in the bilateral entorhinal cortices and hippocampi. Our results suggest that hypermetabolism in the somatomotor cortex, posterior putamen, or central cerebellum could be a useful imaging biomarker for detecting DLB patients, while entorhinal/hippocampal hypometabolism could be a specific biomarker for AD.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier-
dc.relation.isPartOfNEUROBIOLOGY OF AGING-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleDistinguishing between dementia with Lewy bodies and Alzheimer's disease using metabolic patterns-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Neurology (신경과학교실)-
dc.contributor.googleauthorByoung Seok Ye-
dc.contributor.googleauthorSangwon Lee-
dc.contributor.googleauthorHansoo Yoo-
dc.contributor.googleauthorSeok Jong Chung-
dc.contributor.googleauthorYang Hyun Lee-
dc.contributor.googleauthorYonghoon Choi-
dc.contributor.googleauthorPhil Hyu Lee-
dc.contributor.googleauthorYoung H. Sohn-
dc.contributor.googleauthorMijin Yun-
dc.identifier.doi10.1016/j.neurobiolaging.2019.10.020-
dc.contributor.localIdA01982-
dc.contributor.localIdA04603-
dc.contributor.localIdA05367-
dc.contributor.localIdA02550-
dc.contributor.localIdA05714-
dc.contributor.localIdA03270-
dc.contributor.localIdA04666-
dc.relation.journalcodeJ02322-
dc.identifier.eissn1558-1497-
dc.identifier.pmid31791660-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0197458019303847-
dc.subject.keywordAlzheimer's disease-
dc.subject.keywordAmyloid-β-
dc.subject.keywordDementia with Lewy bodies-
dc.subject.keywordFluorodeoxyglucose positron emission tomography-
dc.subject.keywordMetabolism-
dc.contributor.alternativeNameSohn, Young Ho-
dc.contributor.affiliatedAuthor손영호-
dc.contributor.affiliatedAuthor예병석-
dc.contributor.affiliatedAuthor유한수-
dc.contributor.affiliatedAuthor윤미진-
dc.contributor.affiliatedAuthor이양현-
dc.contributor.affiliatedAuthor이필휴-
dc.contributor.affiliatedAuthor정석종-
dc.citation.volume87-
dc.citation.startPage11-
dc.citation.endPage17-
dc.identifier.bibliographicCitationNEUROBIOLOGY OF AGING, Vol.87 : 11-17, 2020-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Nuclear Medicine (핵의학교실) > 1. Journal Papers

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