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dc.contributor.authorBernabeu-Zornoza, Adela 
dc.contributor.authorCoronel, Raquel 
dc.contributor.authorPalmer, Charlotte 
dc.contributor.authorLopez-Alonso, Victoria 
dc.contributor.authorListe-Noya, Isabel 
dc.date.accessioned2021-09-14T12:03:36Z
dc.date.available2021-09-14T12:03:36Z
dc.date.issued2021-09-02
dc.identifier.citationInt J Mol Sci . 2021 Sep 2;22(17):9537.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/13388
dc.description.abstractAmyloid-β 42 peptide (Aβ1-42 (Aβ42)) is well-known for its involvement in the development of Alzheimer's disease (AD). Aβ42 accumulates and aggregates in fibers that precipitate in the form of plaques in the brain causing toxicity; however, like other forms of Aβ peptide, the role of these peptides remains unclear. Here we analyze and compare the effects of oligomeric and fibrillary Aβ42 peptide on the biology (cell death, proliferative rate, and cell fate specification) of differentiating human neural stem cells (hNS1 cell line). By using the hNS1 cells we found that, at high concentrations, oligomeric and fibrillary Aβ42 peptides provoke apoptotic cellular death and damage of DNA in these cells, but Aβ42 fibrils have the strongest effect. The data also show that both oligomeric and fibrillar Aβ42 peptides decrease cellular proliferation but Aβ42 oligomers have the greatest effect. Finally, both, oligomers and fibrils favor gliogenesis and neurogenesis in hNS1 cells, although, in this case, the effect is more prominent in oligomers. All together the findings of this study may contribute to a better understanding of the molecular mechanisms involved in the pathology of AD and to the development of human neural stem cell-based therapies for AD treatment.es_ES
dc.description.sponsorshipThis work was supported by grants from the Spanish Ministry of Science and Innovation (RTI2018-101663-B-100), MICINN-ISCIII (PI-10/00291 and MPY1412/09), MINECO (SAF2015-71140-R), and Comunidad de Madrid (NEUROSTEMCM consortium; S2010/BMD-2336).es_ES
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI)es_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectAlzheimer’ses_ES
dc.subjectAβ peptidees_ES
dc.subjectAβ42.es_ES
dc.subjectCell deathes_ES
dc.subjectCell differentiationes_ES
dc.subjectFibrilses_ES
dc.subjectHuman NSCses_ES
dc.subjectOligomerses_ES
dc.titleOligomeric and Fibrillar Species of Aβ42 Diversely Affect Human Neural Stem Cells.es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID34502444es_ES
dc.format.volume22es_ES
dc.format.number17es_ES
dc.format.page9537es_ES
dc.identifier.doi10.3390/ijms22179537es_ES
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderComunidad de Madrid
dc.description.peerreviewedes_ES
dc.identifier.e-issn1422-0067es_ES
dc.relation.publisherversionhttps://doi.org/10.3390/ijms22179537es_ES
dc.identifier.journalInternational Journal of Molecular Scienceses_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/RTI2018-101663-B-100es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SAF2015-71140-Res_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/MPY1412/09es_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/PI-10/00291es_ES


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