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Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases

DC Field Value Language
dc.contributor.author류철형-
dc.contributor.author유영훈-
dc.contributor.author이명식-
dc.contributor.author이승하-
dc.contributor.author이재훈-
dc.contributor.author조한나-
dc.contributor.author최재용-
dc.date.accessioned2018-08-28T16:53:41Z-
dc.date.available2018-08-28T16:53:41Z-
dc.date.issued2018-
dc.identifier.issn0885-3185-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/162045-
dc.description.abstractBACKGROUND: In addition to Lewy body pathology, amyloid-beta plaques and neurofibrillary tangles that are characteristic for Alzheimer's disease are also frequently found in Lewy body diseases. OBJECTIVES: The objective of this study was to investigate tau accumulation patterns in dementia with Lewy bodies and other Lewy body diseases using in vivo (18) F-AV-1451 PET. METHODS: The study included 12 Parkinson's disease (PD) patients with normal cognition, 22 PD patients with cognitive impairment, and 18 dementia with Lewy bodies patients. In addition, 25 Alzheimer's disease patients and 25 healthy controls were included for comparison. All participants underwent (18) F-AV-1451 and (18) F-florbetaben PET scans, and cortical binding values were compared between the controls and each disease group. RESULTS: When compared with the controls, dementia with Lewy bodies patients showed slightly increased (18) F-AV-1451 binding in the primary sensorimotor and visual cortices and the parieto-temporal cortices, which failed to survive multiple comparisons. Amyloid-positive dementia with Lewy bodies patients showed significantly increased binding in the same regions when compared with controls, and even greater binding in the primary sensorimotor and visual cortices than Alzheimer's disease. Meanwhile, binding in the lateral and medial temporal cortices was less prominent than in Alzheimer's disease. In dementia with Lewy bodies, (18) F-AV-1451 binding in the occipital cortex correlated with (18) F-florbetaben binding. Amyloid-negative patients with normal cognition, patients with cognitive impairment, and dementia with Lewy bodies patients did not show increased (18) F-AV-1451 binding. CONCLUSIONS: Dementia with Lewy bodies patients may harbor (18) F-AV-1451 binding patterns distinct from Alzheimer's disease, with greater involvement of the primary cortices and less involvement of the temporal cortex. Tau burden increases in the Lewy body disease spectrum, and amyloid may play an important role in the accumulation of neocortical tau in Lewy body diseases. (c) 2017 International Parkinson and Movement Disorder Society.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherWiley-Liss-
dc.relation.isPartOfMOVEMENT DISORDERS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleDistinct patterns of amyloid-dependent tau accumulation in Lewy body diseases-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Neurology-
dc.contributor.googleauthorSeung Ha Lee-
dc.contributor.googleauthorHanna Cho-
dc.contributor.googleauthorJae Yong Choi-
dc.contributor.googleauthorJae Hoon Lee-
dc.contributor.googleauthorYoung Hoon Ryu-
dc.contributor.googleauthorMyung Sik Lee-
dc.contributor.googleauthorChul Hyoung Lyoo-
dc.identifier.doi10.1002/mds.27252-
dc.contributor.localIdA01333-
dc.contributor.localIdA02485-
dc.contributor.localIdA02753-
dc.contributor.localIdA04628-
dc.contributor.localIdA03093-
dc.contributor.localIdA03920-
dc.contributor.localIdA04695-
dc.relation.journalcodeJ02275-
dc.identifier.eissn1531-8257-
dc.identifier.pmid29168583-
dc.identifier.urlhttps://onlinelibrary.wiley.com/doi/abs/10.1002/mds.27252-
dc.subject.keyword18F-AV-1451-
dc.subject.keywordtau-
dc.subject.keywordpositron emission tomography-
dc.subject.keywordLewy body disease-
dc.subject.keyworddementia with Lewy bodies-
dc.contributor.alternativeNameLyoo, Chul Hyoung-
dc.contributor.alternativeNameRyu, Young Hoon-
dc.contributor.alternativeNameLee, Myung Sik-
dc.contributor.alternativeNameLee, Seung Ha-
dc.contributor.alternativeNameLee, Jae Hoon-
dc.contributor.alternativeNameCho, Hanna-
dc.contributor.alternativeNameChoi, Jae Yong-
dc.contributor.affiliatedAuthorLyoo, Chul Hyoung-
dc.contributor.affiliatedAuthorRyu, Young Hoon-
dc.contributor.affiliatedAuthorLee, Myung Sik-
dc.contributor.affiliatedAuthorLee, Seung Ha-
dc.contributor.affiliatedAuthorLee, Jae Hoon-
dc.contributor.affiliatedAuthorCho, Hanna-
dc.contributor.affiliatedAuthorChoi, Jae Yong-
dc.citation.volume33-
dc.citation.number2-
dc.citation.startPage262-
dc.citation.endPage272-
dc.identifier.bibliographicCitationMOVEMENT DISORDERS, Vol.33(2) : 262-272, 2018-
dc.identifier.rimsid59635-
dc.type.rimsART-
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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