373 482

Cited 55 times in

Effect of APOE ε4 genotype on amyloid-β and tau accumulation in Alzheimer's disease

DC Field Value Language
dc.contributor.author류철형-
dc.contributor.author백민석-
dc.contributor.author유영훈-
dc.contributor.author이재훈-
dc.contributor.author이혜선-
dc.contributor.author조한나-
dc.date.accessioned2020-12-01T18:00:55Z-
dc.date.available2020-12-01T18:00:55Z-
dc.date.issued2020-10-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/180555-
dc.description.abstractBackground: To assess the effects of apolipoprotein E (ApoE) ε4 genotype on amyloid-β (Aβ) and tau burden and their longitudinal changes in Alzheimer's disease (AD) spectrum. Methods: Among 272 individuals who underwent PET scans (18F-florbetaben for Aβ and 18F-flortaucipir for tau) and ApoE genotyping, 187 individuals completed 2-year follow-up PET scans. After correcting for the partial volume effect, we compared the standardized uptake value ratio (SUVR) for Aβ and tau burden between the ε4+ and ε4- groups. By using a linear mixed-effect model, we measured changes in SUVR in the ApoE ε4+ and ε4- groups. Results: The ε4+ group showed greater baseline Aβ burden in the diffuse cortical regions and greater tau burden in the lateral, and medial temporal, cingulate, and insula cortices. Tau accumulation rate was higher in the parietal, occipital, lateral, and medial temporal cortices in the ε4+ group. In Aβ+ individuals, baseline tau burden was greater in the medial temporal cortex, while Aβ burden was conversely greater in the ε4- group. Tau accumulation rate was higher in the ε4+ group in a small region in the lateral temporal cortex. The effect of ApoE ε4 on enhanced tau accumulation persisted even after adjusting for the global cortical Aβ burden. Conclusions: Progressive tau accumulation may be more prominent in ε4 carriers, particularly in the medial and lateral temporal cortices. ApoE ε4 allele has differential effects on the Aβ burden depending on the existing amyloidosis and may enhance vulnerability to progressive tau accumulation in the AD spectrum independent of Aβ.-
dc.description.statementOfResponsibilityopen-
dc.languageALZHEIMERS RESEARCH & THERAPY-
dc.publisherALZHEIMERS RESEARCH & THERAPY-
dc.relation.isPartOfALZHEIMERS RESEARCH & THERAPY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleEffect of APOE ε4 genotype on amyloid-β and tau accumulation in Alzheimer's disease-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Neurology (신경과학교실)-
dc.contributor.googleauthorMin Seok Baek-
dc.contributor.googleauthorHanna Cho-
dc.contributor.googleauthorHye Sun Lee-
dc.contributor.googleauthorJae Hoon Lee-
dc.contributor.googleauthorYoung Hoon Ryu-
dc.contributor.googleauthorChul Hyoung Lyoo-
dc.identifier.doi10.1186/s13195-020-00710-6-
dc.contributor.localIdA01333-
dc.contributor.localIdA04947-
dc.contributor.localIdA02485-
dc.contributor.localIdA03093-
dc.contributor.localIdA03312-
dc.contributor.localIdA03920-
dc.relation.journalcodeJ03592-
dc.identifier.eissn1758-9193-
dc.identifier.pmid33129364-
dc.subject.keywordAlzheimer disease-
dc.subject.keywordAmyloid-β-
dc.subject.keywordApoE-
dc.subject.keywordPositron emission tomography-
dc.subject.keywordTau-
dc.contributor.alternativeNameLyoo, Chul Hyoung-
dc.contributor.affiliatedAuthor류철형-
dc.contributor.affiliatedAuthor백민석-
dc.contributor.affiliatedAuthor유영훈-
dc.contributor.affiliatedAuthor이재훈-
dc.contributor.affiliatedAuthor이혜선-
dc.contributor.affiliatedAuthor조한나-
dc.citation.volume12-
dc.citation.number1-
dc.citation.startPage140-
dc.identifier.bibliographicCitationALZHEIMERS RESEARCH & THERAPY, Vol.12(1) : 140, 2020-10-
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
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.