Restoring synaptic plasticity and memory in mouse models of Alzheimer's disease by PKR inhibition
DC Field | Value | Language |
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dc.contributor.author | Hwang, Kyoung-Doo | - |
dc.contributor.author | Bak, Myeong Seong | - |
dc.contributor.author | Kim, Sang Jeong | - |
dc.contributor.author | Rhee, Sangmyung | - |
dc.contributor.author | Lee, Yong-Seok | - |
dc.date.available | 2019-03-08T07:36:02Z | - |
dc.date.issued | 2017-12 | - |
dc.identifier.issn | 1756-6606 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/3501 | - |
dc.description.abstract | Alzheimer's disease (AD) is a neurodegenerative disorder associated with deficits in cognition and synaptic plasticity. While accumulation of amyloid beta (A beta) and hyper-phosphorylation of tau are parts of the etiology, AD can be caused by a large number of different genetic mutations and other unknown factors. Considering such a heterogeneous nature of AD, it would be desirable to develop treatment strategies that can improve memory irrespective of the individual causes. Reducing the phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2 alpha) was shown to enhance long-term memory and synaptic plasticity in naive mice. Moreover, hyper-phosphorylation of eIF2 alpha is observed in the brains of postmortem AD patients. Therefore, regulating eIF2 alpha phosphorylation can be a plausible candidate for restoring memory in AD by targeting memory-enhancing mechanism. In this study, we examined whether PKR inhibition can rescue synaptic and learning deficits in two different AD mouse models; 5XFAD transgenic and A beta(1-42)-injected mice. We found that the acute treatment of PKR inhibitor (PKRi) can restore the deficits in long-term memory and long-term potentiation (LTP) in both mouse models without affecting the A beta load in the hippocampus. Our results prove the principle that targeting memory enhancing mechanisms can be a valid candidate for developing AD treatment. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | BIOMED CENTRAL LTD | - |
dc.title | Restoring synaptic plasticity and memory in mouse models of Alzheimer's disease by PKR inhibition | - |
dc.type | Article | - |
dc.identifier.doi | 10.1186/s13041-017-0338-3 | - |
dc.identifier.bibliographicCitation | MOLECULAR BRAIN, v.10, no.1 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.wosid | 000417881700001 | - |
dc.identifier.scopusid | 2-s2.0-85037854746 | - |
dc.citation.number | 1 | - |
dc.citation.title | MOLECULAR BRAIN | - |
dc.citation.volume | 10 | - |
dc.type.docType | Article | - |
dc.publisher.location | 영국 | - |
dc.subject.keywordAuthor | Alzheimer's disease (AD) | - |
dc.subject.keywordAuthor | Amyloid beta (A beta) | - |
dc.subject.keywordAuthor | PKR inhibitor (PKRi) | - |
dc.subject.keywordAuthor | Contextual fear conditioning | - |
dc.subject.keywordAuthor | Object recognition memory | - |
dc.subject.keywordAuthor | Long-term potentiation (LTP) | - |
dc.subject.keywordPlus | DORSAL HIPPOCAMPUS | - |
dc.subject.keywordPlus | ENHANCED COGNITION | - |
dc.subject.keywordPlus | EIF2-ALPHA KINASES | - |
dc.subject.keywordPlus | BETA OLIGOMERS | - |
dc.subject.keywordPlus | SPATIAL MEMORY | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | DEFICITS | - |
dc.subject.keywordPlus | RESCUES | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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