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Loss of Hippocampal Calretinin and Parvalbumin Interneurons in the 5XFAD Mouse Model of Alzheimer’s Disease

dc.contributor.authorGiesers, Naomi K.
dc.contributor.authorWirths, Oliver
dc.date.accessioned2020-06-26T14:02:18Z
dc.date.available2020-06-26T14:02:18Z
dc.date.issued2020de
dc.identifier.urihttp://resolver.sub.uni-goettingen.de/purl?gs-1/17410
dc.description.abstractThe deposition of amyloid-b peptides in the form of extracellular plaques and neuronal degeneration belong to the hallmark features of Alzheimer’s disease (AD). In addition, impaired calcium homeostasis and altered levels in calcium-binding proteins seem to be associated with the disease process. In this study, calretinin- (CR) and parvalbumin- (PV) positive gammaaminobutyric acid-producing (GABAergic) interneurons were quantified in different hippocampal subfields of 12-month-old wild-type mice, as well as in the transgenic AD mouse models 5XFAD and Tg4-42. While, in comparison with wild-type mice, CR-positive interneurons were mainly reduced in the CA1 and CA2/3 regions in plaque-bearing 5XFAD mice, PV-positive interneurons were reduced in all analyzed subfields including the dentate gyrus. No reduction in CR- and PV-positive interneuron numbers was detected in the non-plaque-forming Tg4-42 mouse, although this model has been previously demonstrated to harbor a massive loss of CA1 pyramidal neurons. These results provide information about hippocampal interneuron numbers in two relevant AD mouse models, suggesting that interneuron loss in this brain region may be related to extracellular amyloid burden.de
dc.description.sponsorshipOpen-Access-Publikationsfonds 2020
dc.language.isoengde
dc.rightsopenAccess
dc.rightsNamensnennung-Nicht-kommerziell 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/*
dc.subjectalzheimer; transgenic mice; 5XFAD; calretinin; parvalbumin; Abeta; interneuron; hippocampus; Tg4-42de
dc.subject.ddc610
dc.titleLoss of Hippocampal Calretinin and Parvalbumin Interneurons in the 5XFAD Mouse Model of Alzheimer’s Diseasede
dc.typejournalArticlede
dc.identifier.doi10.1177/1759091420925356
dc.type.versionpublishedVersionde
dc.relation.pISSN1759-0914
dc.relation.eISSN1759-0914
dc.bibliographicCitation.volume12de
dc.bibliographicCitation.firstPage1de
dc.bibliographicCitation.lastPage12de
dc.type.subtypejournalArticle
dc.bibliographicCitation.articlenumber1759091420925356
dc.description.statuspeerReviewedde
dc.bibliographicCitation.journalASN Neurode


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