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dc.contributor.authorÁlvarez Martín, Javier 
dc.contributor.authorÁlvarez Illera, María Pilar
dc.contributor.authorSanto Domingo Mayoral, Jaime
dc.contributor.authorFonteriz García, Rosalba Inés 
dc.contributor.authorMontero Zoccola, María Teresa 
dc.date.accessioned2024-02-13T15:43:35Z
dc.date.available2024-02-13T15:43:35Z
dc.date.issued2022
dc.identifier.citationBiomedicines, Enero 2022, 10, 288es
dc.identifier.issn2227-9059es
dc.identifier.urihttps://uvadoc.uva.es/handle/10324/66234
dc.descriptionProducción Científicaes
dc.description.abstractAlzheimer’s disease (AD) is the most frequent cause of dementia. After decades of research, we know the importance of the accumulation of protein aggregates such as -amyloid peptide and phosphorylated tau. We also know that mutations in certain proteins generate early-onset Alzheimer’s disease (EOAD), and many other genes modulate the disease in its sporadic form. However, the precise molecular mechanisms underlying AD pathology are still unclear. Because of ethical limitations, we need to use animal models to investigate these processes. The nematode Caenorhabditis elegans has received considerable attention in the last 25 years, since the first AD models overexpressing A peptide were described. We review here the main results obtained using this model to study AD. We include works studying the basic molecular mechanisms of the disease, as well as those searching for new therapeutic targets. Although this model also has important limitations, the ability of this nematode to generate knock-out or overexpression models of any gene, single or combined, and to carry out toxicity, recovery or survival studies in short timeframes with many individuals and at low cost is difficult to overcome. We can predict that its use as a model for various diseases will certainly continue to increase.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherMDPIes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.classificationC. elegans; -amyloid; amyloid precursor protein; tau protein; presenilin; new therapieses
dc.titleModeling Alzheimer’s Disease in Caenorhabditis eleganses
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.3390/biomedicines10020288es
dc.relation.publisherversionhttps://www.mdpi.com/2227-9059/10/2/288es
dc.identifier.publicationfirstpage288es
dc.identifier.publicationtitleBiomedicineses
dc.identifier.publicationvolume10es
dc.peerreviewedSIes
dc.description.projectMICINN project BFU2017-83509-Res
dc.identifier.essn2227-9059es
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones


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