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DC Field | Value | Language |
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dc.contributor.author | Griñán Ferré, Christian | - |
dc.contributor.author | Jarné-Ferrer, Júlia | - |
dc.contributor.author | Bellver-Sanchis, Aina | - |
dc.contributor.author | Ribalta Vilella, Marta | - |
dc.contributor.author | Barroso Fernández, Emma | - |
dc.contributor.author | Salvador, Jesús M. | - |
dc.contributor.author | Jurado Aguilar, Javier | - |
dc.contributor.author | Palomer Tarridas, Francesc Xavier | - |
dc.contributor.author | Vázquez Carrera, Manuel | - |
dc.contributor.author | Pallàs i Llibería, Mercè, 1964- | - |
dc.date.accessioned | 2024-04-16T07:38:42Z | - |
dc.date.available | 2024-04-16T07:38:42Z | - |
dc.date.issued | 2024-02-23 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.uri | http://hdl.handle.net/2445/210000 | - |
dc.description.abstract | <p><em>Gadd45 genes have been implicated in survival mechanisms, including apoptosis, autophagy,</em></p><p><em>cell cycle arrest, and DNA repair, which are processes related to aging and life span. Here, we</em></p><p><em>analyzed if the deletion of Gadd45a activates pathways involved in neurodegenerative disorders such</em></p><p><em>as Alzheimer’s Disease (AD). This study used wild-type (WT) and Gadd45a knockout (Gadd45a−/−)</em></p><p><em>mice to evaluate AD progression. Behavioral tests showed that Gadd45a−/− mice presented lower</em></p><p><em>working and spatial memory, pointing out an apparent cognitive impairment compared with WT</em></p><p><em>animals, accompanied by an increase in Tau hyperphosphorylation and the levels of kinases involved</em></p><p><em>in its phosphorylation in the hippocampus. Moreover, Gadd45a−/− animals significantly increased the</em></p><p><em>brain’s pro-inflammatory cytokines and modified autophagy markers. Notably, neurotrophins and</em></p><p><em>the dendritic spine length of the neurons were reduced in Gadd45a−/− mice, which could contribute</em></p><p><em>to the cognitive alterations observed in these animals. Overall, these findings demonstrate that the</em></p><p><em>lack of the Gadd45a gene activates several pathways that exacerbate AD pathology, suggesting that</em></p><p><em>promoting this protein’s expression or function might be a promising therapeutic strategy to slow</em></p><p><em>down AD progression.</em></p> | - |
dc.format.extent | 1 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | MDPI | - |
dc.relation.isformatof | Reproducció del document publicat a: | - |
dc.relation.ispartof | International Journal of Molecular Sciences, 2024 | - |
dc.rights | cc-by (c) Griñán-Ferré C et al., 2024 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | - |
dc.source | Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica) | - |
dc.subject.classification | Malaltia d'Alzheimer | - |
dc.subject.classification | Malalties neurodegeneratives | - |
dc.subject.classification | Epigenètica | - |
dc.subject.other | Alzheimer's disease | - |
dc.subject.other | Neurodegenerative Diseases | - |
dc.subject.other | Epigenetics | - |
dc.title | Deletion of Gadd45a Expression in Mice Leads to Cognitive and Synaptic Impairment Associated with Alzheimer’s Disease Hallmarks. | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 747771 | - |
dc.date.updated | 2024-04-16T07:38:47Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
Appears in Collections: | Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica) |
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858356.pdf | 3.86 MB | Adobe PDF | View/Open |
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