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Sustained hippocampal neural plasticity questions the reproducibility of an amyloid-β-induced Alzheimer’s disease model

2021Artigo científico Acesso restrito
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dc.contributor.authorPaulo, Sara L
dc.contributor.authorRibeiro Rodrigues, Leonor
dc.contributor.authorRodrigues, Rui S.
dc.contributor.authorMateus, Joana
dc.contributor.authorFonseca-Gomes, João
dc.contributor.authorSoares, Rita
dc.contributor.authorDiógenes, Maria José
dc.contributor.authorSolá, Susana
dc.contributor.authorSebastião, Ana M
dc.contributor.authorRibeiro, Filipa
dc.contributor.authorXapelli, Sara
dc.date.accessioned2022-12-13T12:27:55Z
dc.date.available2022-12-13T12:27:55Z
dc.date.issued2021
dc.description© 2021 – IOS Press. All rights reserved.pt_PT
dc.description.abstractBackground: The use of Alzheimer's disease (AD) models obtained by intracerebral infusion of amyloid-β (Aβ) has been increasingly reported in recent years. Nonetheless, these models may present important challenges. Objective: We have focused on canonical mechanisms of hippocampal-related neural plasticity to characterize a rat model obtained by an intracerebroventricular (icv) injection of soluble amyloid-β42 (Aβ42). Methods: Animal behavior was evaluated in the elevated plus maze, Y-Maze spontaneous or forced alternation, Morris water maze, and open field, starting 2 weeks post-Aβ42 infusion. Hippocampal neurogenesis was assessed 3 weeks after Aβ42 injection. Aβ deposition, tropomyosin receptor kinase B levels, and neuroinflammation were appraised at 3 and 14 days post-Aβ42 administration. Results: We found that immature neuronal dendritic morphology was abnormally enhanced, but proliferation and neuronal differentiation in the dentate gyrus was conserved one month after Aβ42 injection. Surprisingly, animal behavior did not reveal changes in cognitive performance nor in locomotor and anxious-related activity. Brain-derived neurotrophic factor related-signaling was also unchanged at 3 and 14 days post-Aβ icv injection. Likewise, astrocytic and microglial markers of neuroinflammation in the hippocampus were unaltered in these time points. Conclusion: Taken together, our data emphasize a high variability and lack of behavioral reproducibility associated with these Aβ injection-based models, as well as the need for its further optimization, aiming at addressing the gap between preclinical AD models and the human disorder.pt_PT
dc.description.sponsorshipThis research was funded by Fundação para a Ciência e a Tecnologia (FCT)/ Ministério da Ciência, Tecnologia e Ensino Superior (MCTES) através de Fundos do Orçamento de Estado, IF/01227/2015 and UID/BIM/50005/2019. R.S.R. (SFRH/BD/129710/2017), F.F.R. (IMM/CT/35-2018), L.R-R. (IMM/ BI/19-2019), J.F-G. (PD/BD/114441/2016) were in receipt of a fellowship from FCT. This project has received funding from H2020-WIDESPREAD-05- 2017-Twinning (EpiEpinet) under grant agreement No 952455pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationJournal of Alzheimer’s Disease 82 (2021) 1183–1202pt_PT
dc.identifier.doi10.3233/JAD-201567pt_PT
dc.identifier.eissn1875-8908
dc.identifier.issn1387-2877
dc.identifier.urihttp://hdl.handle.net/10451/55377
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherIOP Publishingpt_PT
dc.relationInstituto de Medicina Molecular
dc.relationCB2ExStress: a neurogenic strategy to tackle mood disorders
dc.relationBDNF receptor cleavage:relevance for Alzheimer´s Disease pathophysiology
dc.relationEpileptogenesis and Epilepsy Network: from genes, synapses and circuits to pave the way for novel drugs and strategies
dc.relation.publisherversionhttps://content.iospress.com/journals/journal-of-alzheimers-disease/Pre-press/Pre-presspt_PT
dc.subjectAlzheimer’s diseasept_PT
dc.subjectAmyloid-peptidept_PT
dc.subjectBehaviorpt_PT
dc.subjectHippocampal plasticitypt_PT
dc.subjectMemorypt_PT
dc.titleSustained hippocampal neural plasticity questions the reproducibility of an amyloid-β-induced Alzheimer’s disease modelpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleInstituto de Medicina Molecular
oaire.awardTitleCB2ExStress: a neurogenic strategy to tackle mood disorders
oaire.awardTitleBDNF receptor cleavage:relevance for Alzheimer´s Disease pathophysiology
oaire.awardTitleEpileptogenesis and Epilepsy Network: from genes, synapses and circuits to pave the way for novel drugs and strategies
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/Investigador FCT/IF%2F01227%2F2015%2FCP1317%2FCT0001/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UID%2FBIM%2F50005%2F2019/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F129710%2F2017/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//PD%2FBD%2F114441%2F2016/PT
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/952455/EU
oaire.citation.endPage1202pt_PT
oaire.citation.issue3pt_PT
oaire.citation.startPage1183pt_PT
oaire.citation.titleJournal of Alzheimer's Diseasept_PT
oaire.citation.volume82pt_PT
oaire.fundingStreamInvestigador FCT
oaire.fundingStream6817 - DCRRNI ID
oaire.fundingStreamH2020
person.familyNamePaulo
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person.familyNamede Oliveira Diógenes Nogueira
person.familyNameZeferino Solá da Cruz
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person.givenNameSara
person.givenNameLeonor
person.givenNameRui S
person.givenNameJoana
person.givenNameJoão
person.givenNameRita
person.givenNameMaria José
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person.givenNameAna M
person.givenNameFilipa
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project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
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project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameEuropean Commission
rcaap.rightsrestrictedAccesspt_PT
rcaap.typearticlept_PT
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