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dc.contributor.authorTrujillo-Estrada, Laura
dc.contributor.authorMinh Thu Nguyen, Marie
dc.contributor.authorBaglietto-Vargas, David
dc.contributor.authorLaFerla, Frank
dc.contributor.authorGutierrez-Perez, Antonia 
dc.contributor.authorMoreno-Gonzalez, Ines
dc.contributor.authorSoto, Claudio
dc.contributor.authorShahnawaz, Mohammad
dc.contributor.authorda Cunha, Celia
dc.contributor.authorForner, Stefania
dc.contributor.authorNunez-Diaz, Cristina
dc.contributor.authorPham Tran, Janine
dc.contributor.authorCheung, Alwin
dc.contributor.authorDo Huynh, Kelly
dc.contributor.authorMartinie, Alessandra C.
dc.date.accessioned2021-03-23T10:42:52Z
dc.date.available2021-03-23T10:42:52Z
dc.date.created2020-12-02
dc.date.issued2020-12-02
dc.identifier.urihttps://hdl.handle.net/10630/21252
dc.description.abstractRecent evidence indicates that Aβ can misfold and aggregate into seeds that structurally corrupt native proteins, mimicking a prion-like process. Several studies using FAD animal models have demonstrated that intracerebral infusion of brain extracts from APP-transgenic mice or AD patients induce Aβ deposition and cerebral amyloid angiopathy. To carry out most of these Aβ-seeding studies, APP-transgenic animal have been used. Nevertheless, it remains to be elucidated whether Aβ deposition can be induced by Aβ-seeds in a sporadic AD model that does not overexpress APP and produces wild type human Aβ. We used an innovative model to better understand the amyloidogenic events that occur in sporadic AD. This hAβ-KI model, expresses wild-type human Aβ under the control of the endogenous mouse APP gene. Aβ-seeds from AD patients (stage C) from the AD Research Center (UCI) were administered into 7-8-month-old hAβ-KI and as positive controls 3xTg-AD mice were employed. We demonstrated that amyloid seeds can stimulate Aβ aggregations in 3xTg-AD and hAβ-KI models. We found that Aβ aggregates occur earlier in the 3xTg-AD vs hAβ-KI and that a longer term of treatment is necessary to accelerate diffusible Aβ pathology in the hAβ-KI mice. Thereferoe, this hAβ-KI model represents an important step towards the development of next-generation animal models that will provide better predictive outcomes for human patients.es_ES
dc.description.sponsorshipUCI MIND Pilot project (DBV), Ministry of Science PID2019-108911RA-100 (DBV), U54 AG054349 (FML), Institute of Health Carlos III PI18/01557 (AG) co-financed by FEDER funds (European Union), NIH/NIA Grant P50 AG16573 (UCI-ADRC), Universidad de Málaga, Campus de Excelencia Internacional Andalucía Tech.es_ES
dc.language.isoenges_ES
dc.publisherCold Spring Harbor Laboratoryes_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.subjectVasos sanguíneos - Enfermedades - Congresoses_ES
dc.subjectGlucoproteínas - Congresoses_ES
dc.subject.otherAlzheimer´s diseasees_ES
dc.subject.otherTransgenic micees_ES
dc.subject.otherAmyloides_ES
dc.subject.otherSeedes_ES
dc.subject.otherPropagationes_ES
dc.titleAmyloid-β seeding and propagation processes in a hAβ-KI model of Alzheimer's diseasees_ES
dc.typeinfo:eu-repo/semantics/conferenceObjectes_ES
dc.centroFacultad de Cienciases_ES
dc.relation.eventtitleNEURODEGENERATIVE DISEASES: BIOLOGY & THERAPEUTICSes_ES
dc.relation.eventplaceVirtual eventes_ES
dc.relation.eventdateDecember 2-4es_ES


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