Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Ricobaraza, A. (Ana) | - |
dc.creator | Cuadrado-Tejedor, M. (Mar) | - |
dc.creator | Perez-Mediavilla, L.A. (Luis Alberto) | - |
dc.creator | Frechilla, D. (Diana) | - |
dc.creator | Rio, J. (Joaquín) del | - |
dc.creator | Garcia-Osta, A. (Ana) | - |
dc.date.accessioned | 2011-02-10T15:36:02Z | - |
dc.date.available | 2011-02-10T15:36:02Z | - |
dc.date.issued | 2009-06 | - |
dc.identifier.citation | Ricobaraza A, Cuadrado-Tejedor M, Perez-Mediavilla A, Frechilla D, Del Rio J, Garcia-Osta A. Phenylbutyrate ameliorates cognitive deficit and reduces tau pathology in an Alzheimer's disease mouse model. Neuropsychopharmacology 2009 Jun;34(7):1721-1732. | es_ES |
dc.identifier.issn | 0893-133X | - |
dc.identifier.uri | https://hdl.handle.net/10171/16437 | - |
dc.description.abstract | Chromatin modification through histone acetylation is a molecular pathway involved in the regulation of transcription underlying memory storage. Sodium 4-phenylbutyrate (4-PBA) is a well-known histone deacetylase inhibitor, which increases gene transcription of a number of genes, and also exerts neuroprotective effects. In this study, we report that administration of 4-PBA reversed spatial learning and memory deficits in an established mouse model of Alzheimer’s disease (AD) without altering b-amyloid burden. We also observed that the phosphorylated form of tau was decreased in the AD mouse brain after 4-PBA treatment, an effect probably due to an increase in the inactive form of the glycogen synthase kinase 3b (GSK3b). Interestingly, we found a dramatic decrease in brain histone acetylation in the transgenic mice that may reflect an indirect transcriptional repression underlying memory impairment. The administration of 4-PBA restored brain histone acetylation levels and, as a most likely consequence, activated the transcription of synaptic plasticity markers such as the GluR1 subunit of the AMPA receptor, PSD95, and microtubule-associated protein-2. The results suggest that 4-PBA, a drug already approved for clinical use, may provide a novel approach for the treatment of AD. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Nature Publishing Group | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | Alzheimer’s disease | es_ES |
dc.subject | Phenylbutyrate | es_ES |
dc.subject | Histone deacetylase | es_ES |
dc.subject | GSK3b | es_ES |
dc.subject | Memory | es_ES |
dc.title | Phenylbutyrate ameliorates cognitive deficit and reduces tau pathology in an Alzheimer's disease mouse model | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.identifier.doi | http://dx.doi.org/10.1038/npp.2008.229 | es_ES |
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