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Article: Hyper-expression of human apolipoprotein E4 in astroglia and neurons does not enhance amyloid deposition in transgenic mice

TitleHyper-expression of human apolipoprotein E4 in astroglia and neurons does not enhance amyloid deposition in transgenic mice
Authors
Issue Date2001
PublisherOxford University Press. The Journal's web site is located at http://hmg.oxfordjournals.org/
Citation
Human Molecular Genetics, 2001, v. 10 n. 22, p. 2525-2537 How to Cite?
AbstractRecent studies in mice have clearly demonstrated that eliminating Apo E alters the rate, character and distribution of Aβ deposits. In the present study, we asked whether elevating the levels of Apo E can, in a dominant fashion, influence amyloid deposition. We expressed human (Hu) Apo E4 via the mouse prion protein promoter, resulting in high expression in both astrocytes and neurons; only astrocytes efficiently secreted Hu Apo E4 (at least 5-fold more than endogenous). Mice hyper-expressing Hu Apo E4 developed normally and lived normal lifespans. The co-expression of Hu Apo E4 with a mutant amyloid precursor protein (APP) (Mo/Hu APPswe) or mutant APP and mutant presenilin (PS1dE9) did not lead to proportional changes in the age of appearance, relative burden, character or distribution of Aβ deposits. We suggest that these data are best explained by proposing that the mechanisms by which Apo E influences Aβ deposition involves an aspect of its normal function that is not augmented by hyper-expression.
Persistent Identifierhttp://hdl.handle.net/10722/171699
ISSN
2015 Impact Factor: 5.985
2015 SCImago Journal Rankings: 4.288
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLesuisse, Cen_US
dc.contributor.authorXu, Gen_US
dc.contributor.authorAnderson, Jen_US
dc.contributor.authorWong, Men_US
dc.contributor.authorJankowsky, Jen_US
dc.contributor.authorHoltz, Gen_US
dc.contributor.authorGonzalez, Ven_US
dc.contributor.authorWong, PCYen_US
dc.contributor.authorPrice, DLen_US
dc.contributor.authorTang, Fen_US
dc.contributor.authorWagner, Sen_US
dc.contributor.authorBorchelt, DRen_US
dc.date.accessioned2012-10-30T06:16:28Z-
dc.date.available2012-10-30T06:16:28Z-
dc.date.issued2001en_US
dc.identifier.citationHuman Molecular Genetics, 2001, v. 10 n. 22, p. 2525-2537en_US
dc.identifier.issn0964-6906en_US
dc.identifier.urihttp://hdl.handle.net/10722/171699-
dc.description.abstractRecent studies in mice have clearly demonstrated that eliminating Apo E alters the rate, character and distribution of Aβ deposits. In the present study, we asked whether elevating the levels of Apo E can, in a dominant fashion, influence amyloid deposition. We expressed human (Hu) Apo E4 via the mouse prion protein promoter, resulting in high expression in both astrocytes and neurons; only astrocytes efficiently secreted Hu Apo E4 (at least 5-fold more than endogenous). Mice hyper-expressing Hu Apo E4 developed normally and lived normal lifespans. The co-expression of Hu Apo E4 with a mutant amyloid precursor protein (APP) (Mo/Hu APPswe) or mutant APP and mutant presenilin (PS1dE9) did not lead to proportional changes in the age of appearance, relative burden, character or distribution of Aβ deposits. We suggest that these data are best explained by proposing that the mechanisms by which Apo E influences Aβ deposition involves an aspect of its normal function that is not augmented by hyper-expression.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://hmg.oxfordjournals.org/en_US
dc.relation.ispartofHuman Molecular Geneticsen_US
dc.rightsHuman molecular Genetics. Copyright © Oxford University Press.-
dc.subject.meshAmyloid Beta-Peptides - Metabolismen_US
dc.subject.meshAmyloid Beta-Protein Precursor - Genetics - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApolipoprotein E4en_US
dc.subject.meshApolipoproteins E - Genetics - Metabolismen_US
dc.subject.meshAstrocytes - Cytology - Metabolismen_US
dc.subject.meshBrain - Metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoblottingen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshMutationen_US
dc.subject.meshNeurons - Cytology - Metabolismen_US
dc.subject.meshTime Factorsen_US
dc.titleHyper-expression of human apolipoprotein E4 in astroglia and neurons does not enhance amyloid deposition in transgenic miceen_US
dc.typeArticleen_US
dc.identifier.emailTang, F:ftang@hkucc.hku.hken_US
dc.identifier.authorityTang, F=rp00327en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/hmg/10.22.2525-
dc.identifier.pmid11709540-
dc.identifier.scopuseid_2-s2.0-0035888598en_US
dc.identifier.hkuros72021-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035888598&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume10en_US
dc.identifier.issue22en_US
dc.identifier.spage2525en_US
dc.identifier.epage2537en_US
dc.identifier.isiWOS:000172446300007-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLesuisse, C=7801365551en_US
dc.identifier.scopusauthoridXu, G=7404264099en_US
dc.identifier.scopusauthoridAnderson, J=7406783178en_US
dc.identifier.scopusauthoridWong, M=36985740400en_US
dc.identifier.scopusauthoridJankowsky, J=6602821349en_US
dc.identifier.scopusauthoridHoltz, G=7006381665en_US
dc.identifier.scopusauthoridGonzalez, V=35962604900en_US
dc.identifier.scopusauthoridWong, PCY=7403980430en_US
dc.identifier.scopusauthoridPrice, DL=35353856000en_US
dc.identifier.scopusauthoridTang, F=7201979770en_US
dc.identifier.scopusauthoridWagner, S=7402232858en_US
dc.identifier.scopusauthoridBorchelt, DR=7005319619en_US

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