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Cited 5 time in webofscience Cited 6 time in scopus
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Endogenous amyloid-beta mediates memory forgetting in the normal brain

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dc.contributor.authorLee, Sukwon-
dc.contributor.authorKim, Jeongyeon-
dc.contributor.authorChoi, Sukwoo-
dc.date.accessioned2023-08-16T09:49:37Z-
dc.date.available2023-08-16T09:49:37Z-
dc.date.created2022-01-11-
dc.date.issued2018-11-
dc.identifier.issn0006-291X-
dc.identifier.urihttp://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/720-
dc.description.abstractAmyloid beta (A beta) is known to be one of the strong candidate molecules for initiating Alzheimer's disease and has been extensively studied in the light of disease pathophysiology. However, it is still elusive what roles A beta play in the normal brain. In this study, we report that A beta is required for memory forgetting in the normal brain. We monitored object recognition memory, and in order to quench soluble A beta, we microinjected anti-A beta antibody (4G8) into the ventricles after memory acquisition. Microinjection of anti-A beta antibody prolonged the maintenance of object recognition memory. This effect appeared not to be due to modulation of memory consolidation since antibody injection after memory consolidation still had a similar effect on memory maintenance. Furthermore, the maintenance of object recognition memory was prolonged in Fcgr2b KO mice, which lacks IgG Fc gamma receptor II-b (Fc gamma RIIb), a receptor for soluble A beta oligomers. Taken together, these findings suggest that endogenous A beta is involved in memory forgetting in the normal brain. (C) 2018 Elsevier Inc. All rights reserved.-
dc.language영어-
dc.language.isoen-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.titleEndogenous amyloid-beta mediates memory forgetting in the normal brain-
dc.typeArticle-
dc.contributor.affiliatedAuthorLee, Sukwon-
dc.contributor.affiliatedAuthorKim, Jeongyeon-
dc.identifier.doi10.1016/j.bbrc.2018.10.118-
dc.identifier.scopusid2-s2.0-85056581059-
dc.identifier.wosid000452245200011-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.506, no.3, pp.492 - 497-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.titleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.volume506-
dc.citation.number3-
dc.citation.startPage492-
dc.citation.endPage497-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.subject.keywordPlusSYNAPTIC PLASTICITY-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusRECEPTORS-
dc.subject.keywordPlusCONSOLIDATION-
dc.subject.keywordPlusNEUROTOXICITY-
dc.subject.keywordPlusPREVENTS-
dc.subject.keywordPlusAMYGDALA-
dc.subject.keywordAuthorForgetting-
dc.subject.keywordAuthorLong-term memory-
dc.subject.keywordAuthorAmyloid beta-
dc.subject.keywordAuthorIgG Fc gamma receptor II-b-
dc.subject.keywordAuthorObject recognition memory-
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연구본부 > 정서·인지 질환 연구그룹 > 1. Journal Articles

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연구본부 (뇌발달질환 연구그룹)
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