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dc.contributor.authorEttcheto M.
dc.contributor.authorSánchez-López E.
dc.contributor.authorPons L.
dc.contributor.authorBusquets O.
dc.contributor.authorOlloquequi J.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorPallas M.
dc.contributor.authorGarcía M.L.
dc.contributor.authorAuladell C.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:17:22Z
dc.date.available2020-09-02T22:17:22Z
dc.date.issued2017
dc.identifier10.1016/j.redox.2017.06.003
dc.identifier.citation13, , 345-352
dc.identifier.issn22132317
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4412
dc.descriptionThe aim of the present study is to elucidate the neuronal pathways associated to NSAIDs causing a reduction of the risk and progression of Alzheimer's disease. The research was developed administering the active enantiomer of ibuprofen, dexibuprofen (DXI), in order to reduce associated gastric toxicity. DXI was administered from three to six-month-old female APPswe/PS1dE9 mice as a model of familial Alzheimer's disease. DXI treatment reduced the activation of glial cells and the cytokine release involved in the neurodegenerative process, especially TNFα. Moreover, DXI reduced soluble β-amyloid (Aβ1-42) plaque deposition by decreasing APP, BACE1 and facilitating Aβ degradation by enhancing insulin-degrading enzyme. DXI also decreased TAU hyperphosphorylation inhibiting c-Abl/CABLES/p-CDK5 activation signal pathway and prevented spatial learning and memory impairment in transgenic mice. Therefore, chronic DXI treatment could constitute a potential AD-modifying drug, both restoring cognitive functions and reversing multiple brain neuropathological hallmarks. © 2017 The Authors
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectAlzheimer's disease
dc.subjectAPPSwe/PS1dE9
dc.subjectDexibuprofen
dc.subjectHippocampus
dc.subjectInsulin receptor
dc.subjectMemory impairment
dc.subjectMitochondria
dc.subjectTAU
dc.subjectAbelson kinase
dc.subjectamyloid beta protein[1-42]
dc.subjectbeta secretase 1
dc.subjectcyclin dependent kinase 5
dc.subjectdexibuprofen
dc.subjecttau protein
dc.subjectAbelson kinase
dc.subjectamyloid precursor protein
dc.subjectaspartic proteinase
dc.subjectBace1 protein, mouse
dc.subjectCables1 protein, mouse
dc.subjectcarrier protein
dc.subjectCdk5 protein, mouse
dc.subjectcyclin dependent kinase 5
dc.subjectcycline
dc.subjectdexibuprofen
dc.subjectibuprofen
dc.subjectneuroprotective agent
dc.subjectphosphoprotein
dc.subjectpresenilin 1
dc.subjectsecretase
dc.subjecttau protein
dc.subjecttumor necrosis factor
dc.subjectAlzheimer disease
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcell activation
dc.subjectcognition assessment
dc.subjectcontrolled study
dc.subjectdisease course
dc.subjectenzyme linked immunosorbent assay
dc.subjectfemale
dc.subjectglia cell
dc.subjectimmunofluorescence
dc.subjectmale
dc.subjectmemory disorder
dc.subjectmental deterioration
dc.subjectmouse
dc.subjectnerve degeneration
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectprotein degradation
dc.subjectprotein phosphorylation
dc.subjectreal time polymerase chain reaction
dc.subjectsignal transduction
dc.subjectspatial learning
dc.subjecttreatment outcome
dc.subjecttreatment response
dc.subjectWestern blotting
dc.subjectAlzheimer disease
dc.subjectanalogs and derivatives
dc.subjectanimal
dc.subjectbrain
dc.subjectC57BL mouse
dc.subjectcognition
dc.subjectdrug effects
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectsignal transduction
dc.subjectAlzheimer Disease
dc.subjectAmyloid beta-Protein Precursor
dc.subjectAmyloid Precursor Protein Secretases
dc.subjectAnimals
dc.subjectAspartic Acid Endopeptidases
dc.subjectBrain
dc.subjectCarrier Proteins
dc.subjectCognition
dc.subjectCyclin-Dependent Kinase 5
dc.subjectCyclins
dc.subjectFemale
dc.subjectIbuprofen
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectNeuroprotective Agents
dc.subjectPhosphoproteins
dc.subjectPresenilin-1
dc.subjectProto-Oncogene Proteins c-abl
dc.subjectSignal Transduction
dc.subjecttau Proteins
dc.subjectTumor Necrosis Factor-alpha
dc.titleDexibuprofen prevents neurodegeneration and cognitive decline in APPswe/PS1dE9 through multiple signaling pathways
dc.typeArticle


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