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Regional amyloid PET asymmetry and long-term clinical trajectory in mild cognitive impairment

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dc.contributor.authorLee, Yunjin-
dc.contributor.authorKang, Sungwoo-
dc.contributor.authorKim, Yong Sung-
dc.contributor.authorKim, June Sic-
dc.contributor.authorKim, Hee-Jin-
dc.date.accessioned2026-07-07T04:30:20Z-
dc.date.available2026-07-07T04:30:20Z-
dc.date.issued2026-06-
dc.identifier.issn2352-8729-
dc.identifier.issn2352-8729-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/218201-
dc.description.abstractINTRODUCTION: Hemispheric amyloid positron emission tomography(PET) asymmetry may capture prognostic information beyond binary amyloid status in amnestic mild cognitive impairment (aMCI). METHODS: We retrospectively studied 158 aMCI patients with baseline 18F-florbetaben PET and magnetic resonance imaging acquired within 12 months and a mean follow-up of 6.89 +/- 2.63 years. Participants were classified as amyloid beta (Aj3)-stable (n = 67), Aj3-progressor (n =18), Aj3+ stable (n = 33), or Aj3+ progressor (n = 40). Vertex-wise cortical standardized uptake value ratio (SUVR) asymmetry (|AI|) was analyzed using surface-based general linear models adjusted for age, sex, education years, apolipoprotein E E4 carrier status, global cortical SUVR, and clinical follow-up duration. RESULTS: Aj3-MCI progressors showed higher |AI| in the lateral orbitofrontal cortex (790 vertices, cluster-wise p = 0.0002). Aj3+ MCI progressors showed lower |AI| in the lingual gyrus (478 vertices, cluster-wise p = 0.0001). No cross-status contrast yielded a significant cluster in the covariate-adjusted model. DISCUSSION: Amyloid PET asymmetry reflects prognostic heterogeneity in aMCI, with distinct distributional patterns according to amyloid status.-
dc.format.extent10-
dc.language영어-
dc.language.isoENG-
dc.publisherWILEY-
dc.titleRegional amyloid PET asymmetry and long-term clinical trajectory in mild cognitive impairment-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1002/dad2.70394-
dc.identifier.scopusid2-s2.0-105042560138-
dc.identifier.wosid001798025800001-
dc.identifier.bibliographicCitationALZHEIMER'S & DEMENTIA: DIAGNOSIS, ASSESSMENT & DISEASE MONITORING, v.18, no.2, pp 1 - 10-
dc.citation.titleALZHEIMER'S & DEMENTIA: DIAGNOSIS, ASSESSMENT & DISEASE MONITORING-
dc.citation.volume18-
dc.citation.number2-
dc.citation.startPage1-
dc.citation.endPage10-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClassesci-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryClinical Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusALZHEIMERS ASSOCIATION WORKGROUPS-
dc.subject.keywordPlusDIAGNOSTIC GUIDELINES-
dc.subject.keywordPlusNATIONAL INSTITUTE-
dc.subject.keywordPlusBETA PLAQUES-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusDEPOSITION-
dc.subject.keywordPlusPATHOLOGY-
dc.subject.keywordPlusDEMENTIA-
dc.subject.keywordPlusRECOMMENDATIONS-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordAuthorAlzheimer's disease-
dc.subject.keywordAuthoramyloid beta-
dc.subject.keywordAuthorasymmetry index-
dc.subject.keywordAuthormild cognitive impairment-
dc.identifier.urlhttps://alz-journals.onlinelibrary.wiley.com/doi/10.1002/dad2.70394-
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