Endogenous amyloid-beta mediates memory forgetting in the normal brain
DC Field | Value | Language |
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dc.contributor.author | Lee, Sukwon | - |
dc.contributor.author | Kim, Jeongyeon | - |
dc.contributor.author | Choi, Sukwoo | - |
dc.date.accessioned | 2023-08-16T09:49:37Z | - |
dc.date.available | 2023-08-16T09:49:37Z | - |
dc.date.created | 2022-01-11 | - |
dc.date.issued | 2018-11 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/720 | - |
dc.description.abstract | Amyloid 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.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.title | Endogenous amyloid-beta mediates memory forgetting in the normal brain | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Sukwon | - |
dc.contributor.affiliatedAuthor | Kim, Jeongyeon | - |
dc.identifier.doi | 10.1016/j.bbrc.2018.10.118 | - |
dc.identifier.scopusid | 2-s2.0-85056581059 | - |
dc.identifier.wosid | 000452245200011 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.506, no.3, pp.492 - 497 | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 506 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 492 | - |
dc.citation.endPage | 497 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.subject.keywordPlus | SYNAPTIC PLASTICITY | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | RECEPTORS | - |
dc.subject.keywordPlus | CONSOLIDATION | - |
dc.subject.keywordPlus | NEUROTOXICITY | - |
dc.subject.keywordPlus | PREVENTS | - |
dc.subject.keywordPlus | AMYGDALA | - |
dc.subject.keywordAuthor | Forgetting | - |
dc.subject.keywordAuthor | Long-term memory | - |
dc.subject.keywordAuthor | Amyloid beta | - |
dc.subject.keywordAuthor | IgG Fc gamma receptor II-b | - |
dc.subject.keywordAuthor | Object recognition memory | - |
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