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Apolipoprotein E4, amyloid, and cognition in Alzheimer's and Lewy body disease

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dc.contributor.author백경원-
dc.contributor.author손영호-
dc.contributor.author예병석-
dc.contributor.author이양현-
dc.contributor.author이필휴-
dc.contributor.author전세운-
dc.contributor.author정석종-
dc.contributor.author유한수-
dc.date.accessioned2021-12-28T17:15:54Z-
dc.date.available2021-12-28T17:15:54Z-
dc.date.issued2021-10-
dc.identifier.issn0197-4580-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/187016-
dc.description.abstractThe role of apolipoprotein E4 (APOE4) in the risk of Alzheimer's disease (AD) and Lewy body disease (LBD), and their relationship with β-amyloid deposition and cognitive dysfunction, remain unclear. Using amyloid and dopamine transporter imaging, we enrolled 126 controls and 208 patients with typical AD (pure AD and Lewy body variant of AD), AD with dementia with Lewy bodies, or typical LBD (dementia with Lewy bodies with amyloid deposition and pure LBD). APOE4 was associated with an increased risk of all disease subtypes except pure LBD. APOE4 was associated with increased frontal β-amyloid burden, and typical LBD was associated with increased occipital β-amyloid levels through its interaction with APOE4. APOE4 was associated with deteriorated general cognition and memory dysfunction via its interaction with typical LBD and AD, respectively. In conclusion, the impact of APOE4 on disease risk depends on its effects on β-amyloid deposition, and APOE4 is associated with β-amyloid deposition regardless of the clinical diagnosis. However, it interacts with typical LBD to cause occipital β-amyloid deposition.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier-
dc.relation.isPartOfNEUROBIOLOGY OF AGING-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleApolipoprotein E4, amyloid, and cognition in Alzheimer's and Lewy body disease-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Neurology (신경과학교실)-
dc.contributor.googleauthorJin Ho Jung-
dc.contributor.googleauthorSeun Jeon-
dc.contributor.googleauthorKyoungwon Baik-
dc.contributor.googleauthorYang Hyun Lee-
dc.contributor.googleauthorSeok Jong Chung-
dc.contributor.googleauthorHan Soo Yoo-
dc.contributor.googleauthorSeong Ho Jeong-
dc.contributor.googleauthorYoung H Sohn-
dc.contributor.googleauthorPhil Hyu Lee-
dc.contributor.googleauthorByoung Seok Y-
dc.identifier.doi10.1016/j.neurobiolaging.2021.06.004-
dc.contributor.localIdA05133-
dc.contributor.localIdA01982-
dc.contributor.localIdA04603-
dc.contributor.localIdA05714-
dc.contributor.localIdA03270-
dc.contributor.localIdA06105-
dc.contributor.localIdA04666-
dc.relation.journalcodeJ02322-
dc.identifier.eissn1558-1497-
dc.identifier.pmid34242895-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0197458021001949-
dc.subject.keywordAlzheimer's disease-
dc.subject.keywordApolipoprotein E-
dc.subject.keywordCognition-
dc.subject.keywordLewy body disease-
dc.subject.keywordMixed dementia-
dc.subject.keywordβ-amyloid-
dc.contributor.alternativeNameBaik, Kyoungwon-
dc.contributor.affiliatedAuthor백경원-
dc.contributor.affiliatedAuthor손영호-
dc.contributor.affiliatedAuthor예병석-
dc.contributor.affiliatedAuthor이양현-
dc.contributor.affiliatedAuthor이필휴-
dc.contributor.affiliatedAuthor전세운-
dc.contributor.affiliatedAuthor정석종-
dc.citation.volume106-
dc.citation.startPage45-
dc.citation.endPage54-
dc.identifier.bibliographicCitationNEUROBIOLOGY OF AGING, Vol.106 : 45-54, 2021-10-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers

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