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dc.contributor.authorChia-Chen Liu
dc.contributor.authorChih-Wei Tsai
dc.contributor.authorFerenc Deak
dc.contributor.authorJustin Rogers
dc.contributor.authorMichael Penuliar
dc.contributor.authorYou Me Sung
dc.contributor.authorJames N. Maher
dc.contributor.authorYuan Fu
dc.contributor.authorXia Li
dc.contributor.authorHuaxi Xu
dc.contributor.author许华曦
dc.contributor.authorSteven Estus
dc.contributor.authorHyang-Sook Hoe
dc.contributor.authorJohn D. Fryer
dc.contributor.authorTakahisa Kanekiyo
dc.contributor.authorGuojun Bu
dc.contributor.author卜国军
dc.date.accessioned2014-09-30T02:01:49Z
dc.date.available2014-09-30T02:01:49Z
dc.date.issued2014-09-18
dc.identifier.citationNeuron,2014(9)zh_CN
dc.identifier.issn0896-6273
dc.identifier.urihttp://dx.doi.org/10.1016/j.neuron.2014.08.048
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/80490
dc.description该课题是卜国军教授课题组与美国梅奥医学中心、以及厦门大学神经科学研究所的国家“千人计划”特聘教授许华曦课题组等多位科学家合作完成的。由许华曦和卜国军领导的厦门大学神经科学研究所暨福建省神经退行性疾病及衰老研究重点实验室近年来在神经退行性疾病研究领域取得了一系列优秀的成果,先后在NatMed、NatStructMolBiol、NatRevNeurol、Neuron、ProcNatlAcadSciUSA等国际高水平杂志上以厦门大学为第一署名或通讯单位发表了30多篇SCI论文,总影响因子达250多。zh_CN
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-β. In humans, LRP6 and Wnt signaling are significantly downregulated in AD brains, likely by a mechanism that depends on amyloid-β. Our results define a critical pathway in which decreased LRP6-mediated Wnt signaling, synaptic dysfunction, and elevated Aβ synergistically accelerate AD progression and suggest that restoring LRP6-mediated Wnt signaling can be explored as a viable strategy for AD therapy.zh_CN
dc.language.isoen_USzh_CN
dc.publisherElsevier Inc.zh_CN
dc.relation.isreferencedbyhttp://news.xmu.edu.cn/s/13/t/542/59/5b/info153947.htmzh_CN
dc.titleDeficiency in LRP6-Mediated Wnt Signaling Contributes to Synaptic Abnormalities and Amyloid Pathology in Alzheimer’s Diseasezh_CN
dc.typeArticlezh_CN


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