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dc.contributorVall d'Hebron Barcelona Hospital Campus
dc.contributor.authorMarazuela Fuentes, Paula
dc.contributor.authorPaez Montserrat, Berta
dc.contributor.authorBonaterra Pastra, Anna
dc.contributor.authorSolé Piñol, Montserrat
dc.contributor.authorHernandez Guillamon, Maria Mar
dc.date.accessioned2022-09-09T08:15:55Z
dc.date.available2022-09-09T08:15:55Z
dc.date.issued2022-04-29
dc.identifier.citationMarazuela P, Paez-Montserrat B, Bonaterra-Pastra A, Solé M, Hernández-Guillamon M. Impact of Cerebral Amyloid Angiopathy in Two Transgenic Mouse Models of Cerebral β-Amyloidosis: A Neuropathological Study. Int J Mol Sci. 2022 Apr 29;23(9):4972.
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/11351/8093
dc.descriptionCerebral microbleeds; Cerebral beta-amyloidosis; Preclinical MRI
dc.description.abstractThe pathological accumulation of parenchymal and vascular amyloid-beta (Aβ) are the main hallmarks of Alzheimer’s disease (AD) and Cerebral Amyloid Angiopathy (CAA), respectively. Emerging evidence raises an important contribution of vascular dysfunction in AD pathology that could partially explain the failure of anti-Aβ therapies in this field. Transgenic mice models of cerebral β-amyloidosis are essential to a better understanding of the mechanisms underlying amyloid accumulation in the cerebrovasculature and its interactions with neuritic plaque deposition. Here, our main objective was to evaluate the progression of both parenchymal and vascular deposition in APP23 and 5xFAD transgenic mice in relation to age and sex. We first showed a significant age-dependent accumulation of extracellular Aβ deposits in both transgenic models, with a greater increase in APP23 females. We confirmed that CAA pathology was more prominent in the APP23 mice, demonstrating a higher progression of Aβ-positive vessels with age, but not linked to sex, and detecting a pronounced burden of cerebral microbleeds (cMBs) by magnetic resonance imaging (MRI). In contrast, 5xFAD mice did not present CAA, as shown by the negligible Aβ presence in cerebral vessels and the occurrence of occasional cMBs comparable to WT mice. In conclusion, the APP23 mouse model is an interesting tool to study the overlap between vascular and parenchymal Aβ deposition and to evaluate future disease-modifying therapy before its translation to the clinic.
dc.language.isoeng
dc.publisherMDPI
dc.relation.ispartofseriesInternational Journal of Molecular Sciences;23(9)
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceScientia
dc.subjectRatolins transgènics
dc.subjectAmiloïdosi
dc.subjectMalalties cerebrovasculars
dc.subject.meshMice, Transgenic
dc.subject.meshCerebral Amyloid Angiopathy
dc.subject.meshAmyloid beta-Peptides
dc.titleImpact of Cerebral Amyloid Angiopathy in Two Transgenic Mouse Models of Cerebral β-Amyloidosis: A Neuropathological Study
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.3390/ijms23094972
dc.subject.decsratones transgénicos
dc.subject.decsangiopatía amiloide cerebral
dc.subject.decspéptidos beta amiloides
dc.relation.publishversionhttps://doi.org/10.3390/ijms23094972
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.audienceProfessionals
dc.contributor.organismesInstitut Català de la Salut
dc.contributor.authoraffiliationLaboratori de Recerca Neurovascular, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain
dc.identifier.pmid35563362
dc.identifier.wos000795229700001
dc.relation.projectidinfo:eu-repo/grantAgreement/ES/PE2017-2020/PI20%2F00465
dc.relation.projectidinfo:eu-repo/grantAgreement/ES/PE2017-2020/RD21%2F0006%2F0007
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess


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