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|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.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.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.publisher||Nature Publishing Group||es_ES|
|dc.title||Phenylbutyrate ameliorates cognitive deficit and reduces tau pathology in an Alzheimer's disease mouse model||es_ES|
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