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dc.contributor.authorGlebov, Konstantin
dc.contributor.authorWalter, J
dc.date.accessioned2019-01-30T12:57:17Z
dc.date.available2019-01-30T12:57:17Z
dc.date.issued2012
dc.identifier.issn1660-2854
dc.identifier.issn1660-2862
dc.identifier.urihttp://hdl.handle.net/10026.1/13248
dc.description.abstract

<jats:p>Population-based studies demonstrated that statins might decrease the risk of developing Alzheimer’s disease (AD). Statins inhibit the 3-hydroxy-3-methyl-glutaryl-coenzyme-A reductase and thereby de novo synthesis of cholesterol. Cell culture and animal studies indicated that cholesterol affects the proteolytic processing of the amyloid precursor protein and the generation of amyloid-β (Aβ). Recently, we have demonstrated that statins can also stimulate the degradation of Aβ. The statin-induced clearance of Aβ could be attributed to increased release of the insulin-degrading enzyme (IDE) via an exosome-related unconventional secretory pathway. Interestingly, this statin-induced secretion of exosome-associated IDE was independent of cellular cholesterol concentrations, but rather caused by impairment of isoprenoid biosynthesis and protein prenylation. We further identified a new hexapeptide sequence in the C-terminal region of IDE, named the SlyX motif that is critically involved in IDE secretion. Taken these findings together, the increased clearance of Aβ by stimulated secretion of IDE might contribute to the protective effects of statins against AD.</jats:p>

dc.format.extent309-312
dc.format.mediumPrint-Electronic
dc.languageen
dc.language.isoeng
dc.publisherS. Karger AG
dc.subjectAlzheimer's disease
dc.subjectMetalloproteinase
dc.subjectUnconventional secretion
dc.subjectInsulin-degrading enzyme
dc.subjectSlyX motif
dc.subjectStatins
dc.titleStatins in Unconventional Secretion of Insulin-Degrading Enzyme and Degradation of the Amyloid-β Peptide
dc.typejournal-article
dc.typeJournal Article
plymouth.author-urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000303660600066&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008
plymouth.issue1-4
plymouth.volume10
plymouth.publication-statusPublished
plymouth.journalNeurodegenerative Diseases
dc.identifier.doi10.1159/000332595
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeSwitzerland
dcterms.dateAccepted2011-08-18
dc.identifier.eissn1660-2862
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1159/000332595
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2012
rioxxterms.typeJournal Article/Review


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