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Tau PET in Alzheimer disease and mild cognitive impairment

DC FieldValueLanguage
dc.contributor.author류철형-
dc.contributor.author최재용-
dc.contributor.author유영훈-
dc.contributor.author이명식-
dc.contributor.author이재훈-
dc.contributor.author이혜미-
dc.contributor.author조한나-
dc.date.accessioned2017-10-26T07:15:42Z-
dc.date.available2017-10-26T07:15:42Z-
dc.date.issued2016-
dc.identifier.issn0028-3878-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/151809-
dc.description.abstractOBJECTIVE: To investigate the topographical distribution of tau pathology and its effect on functional and structural changes in patients with Alzheimer disease (AD) and mild cognitive impairment (MCI) by using (18)F-AV-1451 PET. METHODS: We included 20 patients with AD, 15 patients with MCI, and 20 healthy controls, and performed neuropsychological function tests, MRI, as well as (18)F-florbetaben (for amyloid) and (18)F-AV-1451 (for tau) PET scans. By using the regional volume-of-interest masks extracted from MRIs, regional binding values of standardized uptake value ratios and volumes were measured. We compared regional binding values among 3 diagnostic groups and identified correlations among the regional binding values, performance in each cognitive function test, and regional atrophy. RESULTS: (18)F-AV-1451 binding was increased only in the entorhinal cortex in patients with MCI, while patients with AD exhibited greater binding in most cortical regions. In the 35 patients with MCI and AD, (18)F-AV-1451 binding in most of the neocortex increased with a worsening of global cognitive function. The visual and verbal memory functions were associated with the extent of (18)F-AV-1451 binding, especially in the medial temporal regions. The (18)F-AV-1451 binding also correlated with the severity of regional atrophy of the cerebral cortex. CONCLUSIONS: Tau PET imaging with (18)F-AV-1451 could serve as an in vivo biomarker for the evaluation of AD-related tau pathology and monitoring disease progression. The accumulation of pathologic tau is more closely related to functional and structural deterioration in the AD spectrum than β-amyloid.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherLippincott Williams & Wilkins-
dc.relation.isPartOfNEUROLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAged-
dc.subject.MESHAged, 80 and over-
dc.subject.MESHAlzheimer Disease/diagnostic imaging*-
dc.subject.MESHAlzheimer Disease/metabolism*-
dc.subject.MESHAlzheimer Disease/psychology-
dc.subject.MESHAmyloid beta-Peptides/metabolism-
dc.subject.MESHAniline Compounds-
dc.subject.MESHAtrophy-
dc.subject.MESHCognitive Dysfunction/diagnostic imaging*-
dc.subject.MESHCognitive Dysfunction/metabolism*-
dc.subject.MESHCognitive Dysfunction/psychology-
dc.subject.MESHDisease Progression-
dc.subject.MESHEntorhinal Cortex/diagnostic imaging-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHImage Processing, Computer-Assisted-
dc.subject.MESHMagnetic Resonance Imaging-
dc.subject.MESHMale-
dc.subject.MESHMemory-
dc.subject.MESHNeuropsychological Tests-
dc.subject.MESHPositron-Emission Tomography-
dc.subject.MESHProspective Studies-
dc.subject.MESHRadiopharmaceuticals-
dc.subject.MESHStilbenes-
dc.subject.MESHVision, Ocular-
dc.subject.MESHtau Proteins/metabolism*-
dc.titleTau PET in Alzheimer disease and mild cognitive impairment-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Neurology-
dc.contributor.googleauthorHanna Cho-
dc.contributor.googleauthorJae Yong Choi-
dc.contributor.googleauthorMi Song Hwang-
dc.contributor.googleauthorJae Hoon Lee-
dc.contributor.googleauthorYou Jin Kim-
dc.contributor.googleauthorHye Mi Lee-
dc.contributor.googleauthorChul Hyoung Lyoo-
dc.contributor.googleauthorYoung Hoon Ryu-
dc.contributor.googleauthorMyung Sik Lee-
dc.identifier.doi10.1212/WNL.0000000000002892-
dc.contributor.localIdA04695-
dc.contributor.localIdA02485-
dc.contributor.localIdA02753-
dc.contributor.localIdA03093-
dc.contributor.localIdA05019-
dc.contributor.localIdA03920-
dc.contributor.localIdA01333-
dc.relation.journalcodeJ02340-
dc.identifier.eissn1526-632X-
dc.identifier.pmid27358341-
dc.identifier.urlhttp://www.neurology.org/content/87/4/375.long-
dc.contributor.alternativeNameLyoo, Chul Hyoung-
dc.contributor.alternativeNameChoi, Jae Yong-
dc.contributor.alternativeNameRyu, Young Hoon-
dc.contributor.alternativeNameLee, Myung Sik-
dc.contributor.alternativeNameLee, Jae Hoon-
dc.contributor.alternativeNameLee, Hye Mi-
dc.contributor.alternativeNameCho, Hanna-
dc.contributor.affiliatedAuthorChoi, Jae Yong-
dc.contributor.affiliatedAuthorRyu, Young Hoon-
dc.contributor.affiliatedAuthorLee, Myung Sik-
dc.contributor.affiliatedAuthorLee, Jae Hoon-
dc.contributor.affiliatedAuthorLee, Hye Mi-
dc.contributor.affiliatedAuthorCho, Hanna-
dc.contributor.affiliatedAuthorLyoo, Chul Hyoung-
dc.citation.volume87-
dc.citation.number4-
dc.citation.startPage375-
dc.citation.endPage383-
dc.identifier.bibliographicCitationNEUROLOGY, Vol.87(4) : 375-383, 2016-
dc.date.modified2017-10-24-
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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