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Cited 142 time in webofscience Cited 149 time in scopus
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Deficiency in LRP6-Mediated Wnt Signaling Contributes to Synaptic Abnormalities and Amyloid Pathology in Alzheimer's Disease

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dc.contributor.authorLiu, Chia-Chen-
dc.contributor.authorTsai, Chih-Wei-
dc.contributor.authorDeak, Ferenc-
dc.contributor.authorRogers, Justin-
dc.contributor.authorPenuliar, Michael-
dc.contributor.authorSung, You Me-
dc.contributor.authorMaher, James N.-
dc.contributor.authorFu, Yuan-
dc.contributor.authorLi, Xia-
dc.contributor.authorXu, Huaxi-
dc.contributor.authorEstus, Steven-
dc.contributor.authorHoe, Hyang-Sook-
dc.contributor.authorFryer, John D.-
dc.contributor.authorKanekiyo, Takahisa-
dc.contributor.authorBu, Guojun-
dc.date.accessioned2023-08-16T09:51:38Z-
dc.date.available2023-08-16T09:51:38Z-
dc.date.created2022-01-11-
dc.date.issued2014-10-
dc.identifier.issn0896-6273-
dc.identifier.urihttp://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/887-
dc.description.abstractAlzheimer's disease (AD) is an age-related neurological disorder characterized by synaptic loss and dementia. The low-density lipoprotein receptor-related protein 6 (LRP6) is an essential coreceptor for Wnt signaling, and its genetic variants have been linked to AD risk. Here we report that neuronal LRP6-mediated Wnt signaling is critical for synaptic function and cognition. Conditional deletion of Lrp6 gene in mouse forebrain neurons leads to age-dependent deficits in synaptic integrity and memory. Neuronal LRP6 deficiency in an amyloid mouse model also leads to exacerbated amyloid pathology due to increased APP processing to amyloid-beta. In humans, LRP6 and Wnt signaling are significantly downregulated in AD brains, likely by a mechanism that depends on amyloid-b. Our results define a critical pathway in which decreased LRP6-mediated Wnt signaling, synaptic dysfunction, and elevated Ab synergistically accelerate AD progression and suggest that restoring LRP6-mediated Wnt signaling can be explored as a viable strategy for AD therapy.-
dc.language영어-
dc.language.isoen-
dc.publisherCELL PRESS-
dc.titleDeficiency in LRP6-Mediated Wnt Signaling Contributes to Synaptic Abnormalities and Amyloid Pathology in Alzheimer's Disease-
dc.typeArticle-
dc.contributor.affiliatedAuthorHoe, Hyang-Sook-
dc.identifier.doi10.1016/j.neuron.2014.08.048-
dc.identifier.scopusid2-s2.0-84907985969-
dc.identifier.wosid000342502800011-
dc.identifier.bibliographicCitationNEURON, v.84, no.1, pp.63 - 77-
dc.relation.isPartOfNEURON-
dc.citation.titleNEURON-
dc.citation.volume84-
dc.citation.number1-
dc.citation.startPage63-
dc.citation.endPage77-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusCOMMON GENETIC-VARIATION-
dc.subject.keywordPlusBETA-CATENIN-
dc.subject.keywordPlusLRP6-
dc.subject.keywordPlusRECEPTOR-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusLOW-DENSITY-LIPOPROTEIN-RECEPTOR-RELATED-PROTEIN-6-
dc.subject.keywordPlusDEGENERATION-
dc.subject.keywordPlusTRANSMISSION-
dc.subject.keywordPlusDYSFUNCTION-
dc.subject.keywordPlusGENERATION-
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