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Illite improves memory impairment and reduces A beta level in the Tg-APPswe/PS1dE9 mouse model of Alzheimer's disease through Akt/CREB and GSK-3 beta phosphorylation in the brain

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dc.contributor.authorJeon, Songhee-
dc.contributor.authorPark, Jeong-Eun-
dc.contributor.authorLee, Jinhee-
dc.contributor.authorLiu, Quan Feng-
dc.contributor.authorJeong, Ha Jin-
dc.contributor.authorPak, Sok Cheon-
dc.contributor.authorYi, Sudok-
dc.contributor.authorKim, Myung Hun-
dc.contributor.authorKim, Chan-Wha-
dc.contributor.authorPark, Jung-Keug-
dc.contributor.authorKim, Geun Woo-
dc.contributor.authorKoo, Byung-Soo-
dc.date.accessioned2021-09-04T19:22:37Z-
dc.date.available2021-09-04T19:22:37Z-
dc.date.created2021-06-15-
dc.date.issued2015-02-03-
dc.identifier.issn0378-8741-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/94428-
dc.description.abstractEthnopharmacological relevance: The use of illite in Korean medicine has a long history as a therapeutic agent for various cerebrovascular diseases. According to Dongui Bogam, illite can be used for Qj-tonifying, phlegm dispersing and activation of blood circulation which is an important principle for the treatment of brain-associated diseases. Aim of the study: This study was undertaken to evaluate beneficial effects of illite on the neurodegenerative diseases such as Alzheimer's disease (AD). Material and methods: The transgenic mice of AD, Tg-APPswe/PS1dE9, were fed with 1% or 3% of illite for 3 months. Behavioral, immunological and ELISA analyses were used to assess memory impairment with additional measurement of A beta accumulation and plague deposition in the brain. Other in vitro studies were performed to examine whether illite inhibits the A beta-induced neurotoxicity in human neuroblastoma cell line, SH-SY5Y cells. Results: Illite treatment rescued A beta-induced neurotoxicity on SH-SY5Y cells, which was dependent on the PI3K/Alct activation. Intake of illite improved the A beta-induced memory impairment and suppressed A beta levels and plaque deposition in the brain of Tg-APPswe/PS1dE9 mice. Illite increased CREB, Akt, and GSK-3 beta phosphorylation and suppressed tau phosphorylation in the AD-like brains. Moreover, 1% of illite reduced weight gain and suppressed glucose level in the blood. Conclusion: The present study suggests that illite has the potential to be a useful adjunct as a therapeutic drug for the treatment of AD. (C) 2014 Elsevier Ireland Ltd. All rights reserved.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherELSEVIER IRELAND LTD-
dc.subjectELEMENT-BINDING PROTEIN-
dc.subjectGLYCOGEN-SYNTHASE KINASE-3-
dc.subjectLONG-TERM-MEMORY-
dc.subjectTRANSGENIC MICE-
dc.subjectCOGNITIVE DEFICITS-
dc.subjectDIABETES-MELLITUS-
dc.subjectPRECURSOR PROTEIN-
dc.subjectNEURONAL LOSS-
dc.subjectIN-VIVO-
dc.subjectZINC-
dc.titleIllite improves memory impairment and reduces A beta level in the Tg-APPswe/PS1dE9 mouse model of Alzheimer's disease through Akt/CREB and GSK-3 beta phosphorylation in the brain-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Chan-Wha-
dc.identifier.doi10.1016/j.jep.2014.11.029-
dc.identifier.scopusid2-s2.0-84916897116-
dc.identifier.wosid000348950500008-
dc.identifier.bibliographicCitationJOURNAL OF ETHNOPHARMACOLOGY, v.160, pp.69 - 77-
dc.relation.isPartOfJOURNAL OF ETHNOPHARMACOLOGY-
dc.citation.titleJOURNAL OF ETHNOPHARMACOLOGY-
dc.citation.volume160-
dc.citation.startPage69-
dc.citation.endPage77-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaPlant Sciences-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaIntegrative & Complementary Medicine-
dc.relation.journalWebOfScienceCategoryPlant Sciences-
dc.relation.journalWebOfScienceCategoryChemistry, Medicinal-
dc.relation.journalWebOfScienceCategoryIntegrative & Complementary Medicine-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.subject.keywordPlusELEMENT-BINDING PROTEIN-
dc.subject.keywordPlusGLYCOGEN-SYNTHASE KINASE-3-
dc.subject.keywordPlusLONG-TERM-MEMORY-
dc.subject.keywordPlusTRANSGENIC MICE-
dc.subject.keywordPlusCOGNITIVE DEFICITS-
dc.subject.keywordPlusDIABETES-MELLITUS-
dc.subject.keywordPlusPRECURSOR PROTEIN-
dc.subject.keywordPlusNEURONAL LOSS-
dc.subject.keywordPlusIN-VIVO-
dc.subject.keywordPlusZINC-
dc.subject.keywordAuthorAlzheimer&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorIllite-
dc.subject.keywordAuthorBeta-amyloid-
dc.subject.keywordAuthorLithium-
dc.subject.keywordAuthorCREB-
dc.subject.keywordAuthorAkt-
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