Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease

Abstract BACKGROUND AND PURPOSE: Inhibitors of phosphodiesterase 5 (PDE5) affect signalling pathways by elevating cGMP, which is a second messenger involved in processes of neuroplasticity. In the present study, the effects of the PDE5 inhibitor, sildenafil, on the pathological features of Alzheimer...

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Autores: Garcia-Osta, A. (Ana)|||/items/6a828922-d55a-4aca-9dec-ccfb2a7380f8, Aguirre, N. (Norberto)|||/items/14cf46d2-53c6-4060-a22b-8fb690ad81b3, Franco, R. (Rafael)|||/items/11f971cd-f36c-4f89-b4d5-8269d33e93fc, Garcia-Barroso, C. (C.)|||/items/56d7b5c1-8aab-4cbe-a92a-e7195b50044b, Perez-Roldan, J.M. (J.M.)|||/items/0f6b57cd-a14d-4849-8b89-1fe81450bf7a, Puerta, E. (Elena)|||/items/1dc4716b-b5b8-422b-bd27-2d153f66a3b8, Ricobaraza, A. (Ana)|||/items/a537e067-03df-4041-b520-0d8a5bd924ab, Hervias, I. (Isabel)|||/items/a2bc8f76-2803-4476-bcbc-cb40fc347ac4, Cuadrado-Tejedor, M. (Mar)|||/items/8e19b277-1821-4ae8-9617-975de11dbdd1
Tipo de recurso: artículo
Fecha de publicación:2011
País:España
Institución:Universidad de Navarra
Repositorio:Dadun. Depósito Académico Digital de la Universidad de Navarra
Idioma:inglés
OAI Identifier:oai:dadun.unav.edu:10171/22826
Acceso en línea:https://hdl.handle.net/10171/22826
Access Level:acceso abierto
Palabra clave:BDNF
CDK5
GSK3β
sildenafil
p-tau
Alzheimer's disease
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spelling Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's diseaseGarcia-Osta, A. (Ana)|||/items/6a828922-d55a-4aca-9dec-ccfb2a7380f8Aguirre, N. (Norberto)|||/items/14cf46d2-53c6-4060-a22b-8fb690ad81b3Franco, R. (Rafael)|||/items/11f971cd-f36c-4f89-b4d5-8269d33e93fcGarcia-Barroso, C. (C.)|||/items/56d7b5c1-8aab-4cbe-a92a-e7195b50044bPerez-Roldan, J.M. (J.M.)|||/items/0f6b57cd-a14d-4849-8b89-1fe81450bf7aPuerta, E. (Elena)|||/items/1dc4716b-b5b8-422b-bd27-2d153f66a3b8Ricobaraza, A. (Ana)|||/items/a537e067-03df-4041-b520-0d8a5bd924abHervias, I. (Isabel)|||/items/a2bc8f76-2803-4476-bcbc-cb40fc347ac4Cuadrado-Tejedor, M. (Mar)|||/items/8e19b277-1821-4ae8-9617-975de11dbdd1BDNFCDK5GSK3βsildenafilp-tauAlzheimer's diseaseAbstract BACKGROUND AND PURPOSE: Inhibitors of phosphodiesterase 5 (PDE5) affect signalling pathways by elevating cGMP, which is a second messenger involved in processes of neuroplasticity. In the present study, the effects of the PDE5 inhibitor, sildenafil, on the pathological features of Alzheimer's disease and on memory-related behaviour were investigated. EXPERIMENTAL APPROACH: Sildenafil was administered to the Tg2576 transgenic mouse model of Alzheimer's disease and to age-matched negative littermates (controls). Memory function was analysed using the Morris water maze test and fear conditioning tasks. Biochemical analyses were performed in brain lysates from animals treated with saline or with sildenafil. KEY RESULTS: Treatment of aged Tg2576 animals with sildenafil completely reversed their cognitive impairment. Such changes were accompanied in the hippocampus by a reduction of tau hyperphosphorylation and a decrease in the activity of glycogen synthase kinase 3β (GSK3β) and of cyclin-dependent kinase 5 (CDK5) (p25/p35 ratio). Moreover, sildenafil also increased levels of brain-derived neurotrophic factor (BDNF) and the activity-regulated cytoskeletal-associated protein (Arc) in the hippocampus without any detectable modification of brain amyloid burden. CONCLUSIONS AND IMPLICATIONS: Sildenafil improved cognitive functions in Tg2576 mice and the effect was not related to changes in the amyloid burden. These data further strengthen the potential of sildenafil as a therapeutic agent for Alzheimer's disease.Wiley-BlackwellDadun. Depósito Académico Digital Universidad de Navarra20122012-07-0420112011-12-0120112011-12-01journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/10171/22826reponame:Dadun. Depósito Académico Digital de la Universidad de Navarrainstname:Universidad de NavarraInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:dadun.unav.edu:10171/228262026-06-21T12:47:57Z
dc.title.none.fl_str_mv Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
title Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
spellingShingle Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
Garcia-Osta, A. (Ana)|||/items/6a828922-d55a-4aca-9dec-ccfb2a7380f8
BDNF
CDK5
GSK3β
sildenafil
p-tau
Alzheimer's disease
title_short Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
title_full Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
title_fullStr Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
title_full_unstemmed Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
title_sort Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease
dc.creator.none.fl_str_mv Garcia-Osta, A. (Ana)|||/items/6a828922-d55a-4aca-9dec-ccfb2a7380f8
Aguirre, N. (Norberto)|||/items/14cf46d2-53c6-4060-a22b-8fb690ad81b3
Franco, R. (Rafael)|||/items/11f971cd-f36c-4f89-b4d5-8269d33e93fc
Garcia-Barroso, C. (C.)|||/items/56d7b5c1-8aab-4cbe-a92a-e7195b50044b
Perez-Roldan, J.M. (J.M.)|||/items/0f6b57cd-a14d-4849-8b89-1fe81450bf7a
Puerta, E. (Elena)|||/items/1dc4716b-b5b8-422b-bd27-2d153f66a3b8
Ricobaraza, A. (Ana)|||/items/a537e067-03df-4041-b520-0d8a5bd924ab
Hervias, I. (Isabel)|||/items/a2bc8f76-2803-4476-bcbc-cb40fc347ac4
Cuadrado-Tejedor, M. (Mar)|||/items/8e19b277-1821-4ae8-9617-975de11dbdd1
author Garcia-Osta, A. (Ana)|||/items/6a828922-d55a-4aca-9dec-ccfb2a7380f8
author_facet Garcia-Osta, A. (Ana)|||/items/6a828922-d55a-4aca-9dec-ccfb2a7380f8
Aguirre, N. (Norberto)|||/items/14cf46d2-53c6-4060-a22b-8fb690ad81b3
Franco, R. (Rafael)|||/items/11f971cd-f36c-4f89-b4d5-8269d33e93fc
Garcia-Barroso, C. (C.)|||/items/56d7b5c1-8aab-4cbe-a92a-e7195b50044b
Perez-Roldan, J.M. (J.M.)|||/items/0f6b57cd-a14d-4849-8b89-1fe81450bf7a
Puerta, E. (Elena)|||/items/1dc4716b-b5b8-422b-bd27-2d153f66a3b8
Ricobaraza, A. (Ana)|||/items/a537e067-03df-4041-b520-0d8a5bd924ab
Hervias, I. (Isabel)|||/items/a2bc8f76-2803-4476-bcbc-cb40fc347ac4
Cuadrado-Tejedor, M. (Mar)|||/items/8e19b277-1821-4ae8-9617-975de11dbdd1
author_role author
author2 Aguirre, N. (Norberto)|||/items/14cf46d2-53c6-4060-a22b-8fb690ad81b3
Franco, R. (Rafael)|||/items/11f971cd-f36c-4f89-b4d5-8269d33e93fc
Garcia-Barroso, C. (C.)|||/items/56d7b5c1-8aab-4cbe-a92a-e7195b50044b
Perez-Roldan, J.M. (J.M.)|||/items/0f6b57cd-a14d-4849-8b89-1fe81450bf7a
Puerta, E. (Elena)|||/items/1dc4716b-b5b8-422b-bd27-2d153f66a3b8
Ricobaraza, A. (Ana)|||/items/a537e067-03df-4041-b520-0d8a5bd924ab
Hervias, I. (Isabel)|||/items/a2bc8f76-2803-4476-bcbc-cb40fc347ac4
Cuadrado-Tejedor, M. (Mar)|||/items/8e19b277-1821-4ae8-9617-975de11dbdd1
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Dadun. Depósito Académico Digital Universidad de Navarra
dc.subject.none.fl_str_mv BDNF
CDK5
GSK3β
sildenafil
p-tau
Alzheimer's disease
topic BDNF
CDK5
GSK3β
sildenafil
p-tau
Alzheimer's disease
description Abstract BACKGROUND AND PURPOSE: Inhibitors of phosphodiesterase 5 (PDE5) affect signalling pathways by elevating cGMP, which is a second messenger involved in processes of neuroplasticity. In the present study, the effects of the PDE5 inhibitor, sildenafil, on the pathological features of Alzheimer's disease and on memory-related behaviour were investigated. EXPERIMENTAL APPROACH: Sildenafil was administered to the Tg2576 transgenic mouse model of Alzheimer's disease and to age-matched negative littermates (controls). Memory function was analysed using the Morris water maze test and fear conditioning tasks. Biochemical analyses were performed in brain lysates from animals treated with saline or with sildenafil. KEY RESULTS: Treatment of aged Tg2576 animals with sildenafil completely reversed their cognitive impairment. Such changes were accompanied in the hippocampus by a reduction of tau hyperphosphorylation and a decrease in the activity of glycogen synthase kinase 3β (GSK3β) and of cyclin-dependent kinase 5 (CDK5) (p25/p35 ratio). Moreover, sildenafil also increased levels of brain-derived neurotrophic factor (BDNF) and the activity-regulated cytoskeletal-associated protein (Arc) in the hippocampus without any detectable modification of brain amyloid burden. CONCLUSIONS AND IMPLICATIONS: Sildenafil improved cognitive functions in Tg2576 mice and the effect was not related to changes in the amyloid burden. These data further strengthen the potential of sildenafil as a therapeutic agent for Alzheimer's disease.
publishDate 2011
dc.date.none.fl_str_mv 2011
2011-12-01
2011
2011-12-01
2012
2012-07-04
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/10171/22826
url https://hdl.handle.net/10171/22826
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Wiley-Blackwell
publisher.none.fl_str_mv Wiley-Blackwell
dc.source.none.fl_str_mv reponame:Dadun. Depósito Académico Digital de la Universidad de Navarra
instname:Universidad de Navarra
instname_str Universidad de Navarra
reponame_str Dadun. Depósito Académico Digital de la Universidad de Navarra
collection Dadun. Depósito Académico Digital de la Universidad de Navarra
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