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C-11-PIB PET imaging reveals that amyloid deposition in cases with early-onset Alzheimer's disease in the absence of known mutations retains higher levels of PIB in the basal ganglia

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dc.contributor.authorYoun, Young Chul-
dc.contributor.authorJang, Jae-Won-
dc.contributor.authorHan, Su-Hyun-
dc.contributor.authorKim, HyeRyoun-
dc.contributor.authorSeok, Ju-Won-
dc.contributor.authorByun, Jun Soo-
dc.contributor.authorPark, Kwang-Yeol-
dc.contributor.authorAn, Seong Soo A.-
dc.contributor.authorChun, In Kook-
dc.contributor.authorKim, Sangyun-
dc.date.available2019-03-08T11:57:00Z-
dc.date.issued2017-06-
dc.identifier.issn1178-1998-
dc.identifier.issn1178-1998-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/6247-
dc.description.abstractPurpose: Early-onset Alzheimer's disease (EOAD) has a different pathologic burden and clinical features compared with late-onset Alzheimer's disease(LOAD). We examined the effects of age at onset on the burden and distribution of beta-amyloid in patients with EOAD, in whom well-characterized mutations associated with Alzheimer's disease were absent. Methods: We genotyped ApoE, APP, PSEN1 and PSEN2 in the patients with Alzheimer's disease: 9 patients with EOAD (age <65), 11 with LOAD (age >70) and 8 normal controls (NCs), all of whom had undergone C-11-labeled Pittsburgh compound B-positron emission tomography imaging. Results: Patients with EOAD exhibited higher z scores and larger cluster sizes, and retained higher levels of Pittsburgh compound B in the bilateral thalamus and in some parts of the globus pallidus (P<0.05, false discovery rate). Conclusion: Distribution of amyloid deposition in EOAD outside the context of genetic mutations topographically showed some differences from that in LOAD.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherDOVE MEDICAL PRESS LTD-
dc.titleC-11-PIB PET imaging reveals that amyloid deposition in cases with early-onset Alzheimer's disease in the absence of known mutations retains higher levels of PIB in the basal ganglia-
dc.typeArticle-
dc.identifier.doi10.2147/CIA.S132884-
dc.identifier.bibliographicCitationCLINICAL INTERVENTIONS IN AGING, v.12, pp 1041 - 1048-
dc.description.isOpenAccessN-
dc.identifier.wosid000404348200004-
dc.identifier.scopusid2-s2.0-85024103899-
dc.citation.endPage1048-
dc.citation.startPage1041-
dc.citation.titleCLINICAL INTERVENTIONS IN AGING-
dc.citation.volume12-
dc.type.docTypeArticle-
dc.publisher.location뉴질랜드-
dc.subject.keywordAuthorAlzheimer's disease-
dc.subject.keywordAuthorearly-onset Alzheimer's disease-
dc.subject.keywordAuthoramyloid PET-
dc.subject.keywordAuthorbasal ganglia-
dc.subject.keywordAuthorPittsburgh compound B-
dc.subject.keywordAuthoramyloid-
dc.subject.keywordPlusPATHOLOGY-
dc.subject.keywordPlusCOGNITION-
dc.subject.keywordPlusDEMENTIA-
dc.subject.keywordPlusCARRIERS-
dc.subject.keywordPlusGREATER-
dc.subject.keywordPlusNUCLEI-
dc.subject.keywordPlusBURDEN-
dc.relation.journalResearchAreaGeriatrics & Gerontology-
dc.relation.journalWebOfScienceCategoryGeriatrics & Gerontology-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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