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Sildenafil restores cognitive function independent of Aß burden in an Alzheimer’s disease Mouse model
Authors: Cuadrado-Tejedor, M. (Mar)
Hervias, I. (Isabel)
Puerta, E. (Elena)
Perez-Roldan, J.M. (J.M.)
Ricobaraza, A. (Ana)
Aguirre, N. (Norberto)
Garcia-Osta, A. (Ana)
Keywords: 3-Nitropropionic acid
BDNF
Calpain
CREB
Excitotoxicity
Huntington's disease
Phosphodiesterase 5
Sildenafil
Vardenafi
Issue Date: May-2010
Publisher: ELSEVIER SCIENCE INC
ISBN: 0006-3223
Citation: Cuadrado-Tejedor M, Hervias I, Ricobaraza A, Puerta E, Perez-Roldan JM, Garcia-Barroso C, Franco R, Aguirre N, Garcia-Osta A. Sildenafil restores cognitive function independent of Aß burden in an Alzheimer’s disease Mouse model. Biological psychiatry. NEUROSCIENCES 13/221 (Cuartil 1)
Abstract
In this study we tested whether phosphodiesterase 5 (PDE5) inhibitors, sildenafil and vardenafil, would afford protection against 3-nitropropionic acid (3NP), which produces striatal lesions that closely mimic some of the neuropathological features of Huntington's Disease (HD). The neurotoxin was given over 5 days by constant systemic infusion using osmotic minipumps. Animals treated with PDE5 inhibitors (sildenafil or vardenafil) showed improved neurologic scores, reduced the loss of striatal DARPP-32 protein levels and lesion volumes, and decreased calpain activation produced by 3NP. This protective effect was independent of changes in 3NP-induced succinate dehydrogenase inhibition. Furthermore, striatal p-CREB levels along with the expression of BDNF were significantly increased in sildenafil-treated rats. In summary, PDE5 inhibitors protected against 3NP-induced striatal degeneration by reducing calpain activation and by promoting survival pathways. These data encourage further evaluation of PDE5 inhibitors in transgenic mouse models of HD.
Permanent link: http://hdl.handle.net/10171/13047
Appears in Collections:DA - CIMA - Neurociencias - Neurofarmacología y conducta - Artículos de Revista
DA - Medicina - Anatomía - Artículos de revista

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