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dc.contributor.authorEttcheto M.
dc.contributor.authorAbad S.
dc.contributor.authorPetrov D.
dc.contributor.authorPedrós I.
dc.contributor.authorBusquets O.
dc.contributor.authorSánchez-López E.
dc.contributor.authorCasadesús G.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorCarro E.
dc.contributor.authorAuladell C.
dc.contributor.authorOlloquequi J.
dc.contributor.authorPallàs M.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:17:21Z
dc.date.available2020-09-02T22:17:21Z
dc.date.issued2018
dc.identifier10.1007/s12035-017-0690-4
dc.identifier.citation55, 6, 4885-4895
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4407
dc.descriptionThe molecular basis of memory loss in Alzheimer’s disease (AD), the main cause of senile dementia, is under investigation. In the present study, we have focused on the early hippocampal memory-related changes in APPswe/PS1dE9 (APP/PS1) mice, a well-established mouse model of familial AD. It is well known that molecules like cAMP response element binding (CREB) and binding protein (CBP) play a crucial role in memory consolidation. We analyzed CBP on its transcriptional activity and protein levels, finding a significant downregulation of both of them at 3-month-old mice. In addition, the downregulation of this molecule was associated with a decrease on acetylation levels of histone H3 in the hippocampus of APP/PS1 mice. Moreover, the p-CREB levels, which are important for memory acquisition at 3 months in APP/PS1 mice, were downregulated. Furthermore, we suggest that early neuroinflammation, especially due to the Tnfα gene increased expression, could also be responsible to this process of memory loss. Given all the previously mentioned results, we propose that an early suitable treatment to prevent the evolution of the disease should include a combination of drugs, including anti-inflammatories, which may decrease glial activation and Tnfα levels, and phosphodiesterase inhibitors that increase cAMP levels. © 2017, Springer Science+Business Media, LLC.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectAlzheimer disease
dc.subjectAPPSwe/PS1dE9
dc.subjectCBP
dc.subjectCREB
dc.subjectHippocampus
dc.subjectADAM10 endopeptidase
dc.subjectbeta secretase 1
dc.subjectbrain derived neurotrophic factor
dc.subjectcalcium calmodulin dependent protein kinase
dc.subjectcyclic AMP dependent protein kinase
dc.subjectcyclic AMP responsive element binding protein binding protein
dc.subjecthistone H3
dc.subjectmessenger RNA
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectn methyl dextro aspartic acid receptor 1
dc.subjectn methyl dextro aspartic acid receptor 2
dc.subjectprotein kinase B
dc.subjectprotein kinase C
dc.subjecttumor necrosis factor
dc.subjectunclassified drug
dc.subjectamyloid precursor protein
dc.subjectcyclic AMP responsive element binding protein
dc.subjectcyclic AMP responsive element binding protein binding protein
dc.subjecthistone
dc.subjectpresenilin 1
dc.subjectAlzheimer disease
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectBDNF gene
dc.subjectCBP gene
dc.subjectdown regulation
dc.subjectgene expression
dc.subjectgene expression regulation
dc.subjecthippocampus
dc.subjecthistone acetylation
dc.subjectmale
dc.subjectmemory consolidation
dc.subjectmouse
dc.subjectmouse model
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjectprotein phosphorylation
dc.subjectTNF alpha gene
dc.subjectWestern blotting
dc.subjectwild type
dc.subjectacetylation
dc.subjectAlzheimer disease
dc.subjectanimal
dc.subjectdisease model
dc.subjectgenetics
dc.subjecthippocampus
dc.subjectmemory disorder
dc.subjectmetabolism
dc.subjecttransgenic mouse
dc.subjectAcetylation
dc.subjectAlzheimer Disease
dc.subjectAmyloid beta-Protein Precursor
dc.subjectAnimals
dc.subjectCREB-Binding Protein
dc.subjectCyclic AMP Response Element-Binding Protein
dc.subjectDisease Models, Animal
dc.subjectHippocampus
dc.subjectHistones
dc.subjectMemory Disorders
dc.subjectMice
dc.subjectMice, Transgenic
dc.subjectPresenilin-1
dc.titleEarly Preclinical Changes in Hippocampal CREB-Binding Protein Expression in a Mouse Model of Familial Alzheimer’s Disease
dc.typeArticle


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