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dc.contributor.authorEttcheto, Miren
dc.contributor.authorSánchez-López, Elena
dc.contributor.authorCano, Amanda
dc.contributor.authorCarrasco, Marina
dc.contributor.authorHerrera, Katherine
dc.contributor.authorManzine, Patricia Regina
dc.contributor.authorEspinosa-Jiménez, Triana
dc.contributor.authorBusquets, Oriol
dc.contributor.authorVerdaguer, Ester
dc.contributor.authorOlloquequi, Jordi
dc.contributor.authorAuladell, Carme
dc.contributor.authorFolch, Jaume
dc.date.accessioned2021-08-10T14:28:48Z
dc.date.available2021-08-10T14:28:48Z
dc.date.issued2021-12
dc.identifier10.1186/s13578-021-00646-w
dc.identifier.issn20453701
dc.identifier.urihttps://hdl.handle.net/20.500.12728/9428
dc.description.abstractBackground: Several studies stablished a relationship between metabolic disturbances and Alzheimer´s disease (AD) where inflammation plays a pivotal role. However, mechanisms involved still remain unclear. In the present study, we aimed to evaluate central and peripheral effects of dexibuprofen (DXI) in the progression of AD in APPswe/PS1dE9 (APP/PS1) female mice, a familial AD model, fed with high fat diet (HFD). Animals were fed either with conventional chow or with HFD, from their weaning until their sacrifice, at 6 months. Moreover, mice were divided into subgroups to which were administered drinking water or water supplemented with DXI (20 mg kg−1 d−1) for 3 months. Before sacrifice, body weight, intraperitoneal glucose and insulin tolerance test (IP-ITT) were performed to evaluate peripheral parameters and also behavioral tests to determine cognitive decline. Moreover, molecular studies such as Western blot and RT-PCR were carried out in liver to confirm metabolic effects and in hippocampus to analyze several pathways considered hallmarks in AD. Results: Our studies demonstrate that DXI improved metabolic alterations observed in transgenic animals fed with HFD in vivo, data in accordance with those obtained at molecular level. Moreover, an improvement of cognitive decline and neuroinflammation among other alterations associated with AD were observed such as beta-amyloid plaque accumulation and unfolded protein response. Conclusions: Collectively, evidence suggest that chronic administration of DXI prevents the progression of AD through the regulation of inflammation which contribute to improve hallmarks of this pathology. Thus, this compound could constitute a novel therapeutic approach in the treatment of AD in a combined therapy.es_ES
dc.language.isoenes_ES
dc.publisherBioMed Central Ltdes_ES
dc.subjectAlzheimer´s diseasees_ES
dc.subjectAPPswe/PS1dE9es_ES
dc.subjectCognitive deficitses_ES
dc.subjectDexibuprofenes_ES
dc.subjectHigh fat dietes_ES
dc.subjectMetabolic alterationses_ES
dc.subjectneuroinflammationes_ES
dc.subjectSynapsises_ES
dc.subjectUnfolded protein responsees_ES
dc.subjectβA plaqueses_ES
dc.titleDexibuprofen ameliorates peripheral and central risk factors associated with Alzheimer’s disease in metabolically stressed APPswe/PS1dE9 micees_ES
dc.typeArticlees_ES


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