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Early Preclinical Changes in Hippocampal CREB-Binding Protein Expression in a Mouse Model of Familial Alzheimer’s Disease
dc.contributor.author | Ettcheto M. | |
dc.contributor.author | Abad S. | |
dc.contributor.author | Petrov D. | |
dc.contributor.author | Pedrós I. | |
dc.contributor.author | Busquets O. | |
dc.contributor.author | Sánchez-López E. | |
dc.contributor.author | Casadesús G. | |
dc.contributor.author | Beas-Zarate C. | |
dc.contributor.author | Carro E. | |
dc.contributor.author | Auladell C. | |
dc.contributor.author | Olloquequi J. | |
dc.contributor.author | Pallàs M. | |
dc.contributor.author | Folch J. | |
dc.contributor.author | Camins A. | |
dc.date.accessioned | 2020-09-02T22:17:21Z | |
dc.date.available | 2020-09-02T22:17:21Z | |
dc.date.issued | 2018 | |
dc.identifier | 10.1007/s12035-017-0690-4 | |
dc.identifier.citation | 55, 6, 4885-4895 | |
dc.identifier.issn | 08937648 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4407 | |
dc.description | The 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.iso | en | |
dc.publisher | Humana Press Inc. | |
dc.subject | Alzheimer disease | |
dc.subject | APPSwe/PS1dE9 | |
dc.subject | CBP | |
dc.subject | CREB | |
dc.subject | Hippocampus | |
dc.subject | ADAM10 endopeptidase | |
dc.subject | beta secretase 1 | |
dc.subject | brain derived neurotrophic factor | |
dc.subject | calcium calmodulin dependent protein kinase | |
dc.subject | cyclic AMP dependent protein kinase | |
dc.subject | cyclic AMP responsive element binding protein binding protein | |
dc.subject | histone H3 | |
dc.subject | messenger RNA | |
dc.subject | mitogen activated protein kinase 1 | |
dc.subject | mitogen activated protein kinase 3 | |
dc.subject | n methyl dextro aspartic acid receptor | |
dc.subject | n methyl dextro aspartic acid receptor 1 | |
dc.subject | n methyl dextro aspartic acid receptor 2 | |
dc.subject | protein kinase B | |
dc.subject | protein kinase C | |
dc.subject | tumor necrosis factor | |
dc.subject | unclassified drug | |
dc.subject | amyloid precursor protein | |
dc.subject | cyclic AMP responsive element binding protein | |
dc.subject | cyclic AMP responsive element binding protein binding protein | |
dc.subject | histone | |
dc.subject | presenilin 1 | |
dc.subject | Alzheimer disease | |
dc.subject | animal experiment | |
dc.subject | animal model | |
dc.subject | animal tissue | |
dc.subject | Article | |
dc.subject | BDNF gene | |
dc.subject | CBP gene | |
dc.subject | down regulation | |
dc.subject | gene expression | |
dc.subject | gene expression regulation | |
dc.subject | hippocampus | |
dc.subject | histone acetylation | |
dc.subject | male | |
dc.subject | memory consolidation | |
dc.subject | mouse | |
dc.subject | mouse model | |
dc.subject | nervous system inflammation | |
dc.subject | nonhuman | |
dc.subject | protein expression | |
dc.subject | protein phosphorylation | |
dc.subject | TNF alpha gene | |
dc.subject | Western blotting | |
dc.subject | wild type | |
dc.subject | acetylation | |
dc.subject | Alzheimer disease | |
dc.subject | animal | |
dc.subject | disease model | |
dc.subject | genetics | |
dc.subject | hippocampus | |
dc.subject | memory disorder | |
dc.subject | metabolism | |
dc.subject | transgenic mouse | |
dc.subject | Acetylation | |
dc.subject | Alzheimer Disease | |
dc.subject | Amyloid beta-Protein Precursor | |
dc.subject | Animals | |
dc.subject | CREB-Binding Protein | |
dc.subject | Cyclic AMP Response Element-Binding Protein | |
dc.subject | Disease Models, Animal | |
dc.subject | Hippocampus | |
dc.subject | Histones | |
dc.subject | Memory Disorders | |
dc.subject | Mice | |
dc.subject | Mice, Transgenic | |
dc.subject | Presenilin-1 | |
dc.title | Early Preclinical Changes in Hippocampal CREB-Binding Protein Expression in a Mouse Model of Familial Alzheimer’s Disease | |
dc.type | Article |