Prospects for cannabinoid therapies in basal ganglia disorders

Cannabinoids are promising medicines to slow down disease progression in neurodegenerative disorders including Parkinson's disease (PD) and Huntington's disease (HD), two of the most important disorders affecting the basal ganglia. Two pharmacological profiles have been proposed for cannab...

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Autores: Fernández Ruiz, José Javier, Moreno Martet, Miguel, Rodríguez Cueto, Carmen Aurora, Palomo Garo, Cristina, Gómez Cañas, María, Valdeolivas, Sara, Guaza, Carmen, Romero, Julián, Guzmán Pastor, Manuel, Mechoulam, Raphael, Ramos Atance, José Antonio
Tipo de recurso: artículo
Fecha de publicación:2011
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/93221
Acceso en línea:https://hdl.handle.net/20.500.14352/93221
Access Level:acceso abierto
Palabra clave:61
Basal ganglia
Cannabinoid signalling system
Cannabinoids
CB1 receptors
CB2 receptors
Neurodegeneration
Neuroprotection
Ciencias Biomédicas
Ciencias
24 Ciencias de la Vida
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repository_id_str
spelling Prospects for cannabinoid therapies in basal ganglia disordersFernández Ruiz, José JavierMoreno Martet, MiguelRodríguez Cueto, Carmen AuroraPalomo Garo, CristinaGómez Cañas, MaríaValdeolivas, SaraGuaza, CarmenRomero, JuliánGuzmán Pastor, ManuelMechoulam, RaphaelRamos Atance, José Antonio61Basal gangliaCannabinoid signalling systemCannabinoidsCB1 receptorsCB2 receptorsNeurodegenerationNeuroprotectionCiencias BiomédicasCiencias24 Ciencias de la VidaCannabinoids are promising medicines to slow down disease progression in neurodegenerative disorders including Parkinson's disease (PD) and Huntington's disease (HD), two of the most important disorders affecting the basal ganglia. Two pharmacological profiles have been proposed for cannabinoids being effective in these disorders. On the one hand, cannabinoids like Δ9‐tetrahydrocannabinol or cannabidiol protect nigral or striatal neurons in experimental models of both disorders, in which oxidative injury is a prominent cytotoxic mechanism. This effect could be exerted, at least in part, through mechanisms independent of CB1 and CB2 receptors and involving the control of endogenous antioxidant defences. On the other hand, the activation of CB2 receptors leads to a slower progression of neurodegeneration in both disorders. This effect would be exerted by limiting the toxicity of microglial cells for neurons and, in particular, by reducing the generation of proinflammatory factors. It is important to mention that CB2 receptors have been identified in the healthy brain, mainly in glial elements and, to a lesser extent, in certain subpopulations of neurons, and that they are dramatically up‐regulated in response to damaging stimuli, which supports the idea that the cannabinoid system behaves as an endogenous neuroprotective system. This CB2 receptor up‐regulation has been found in many neurodegenerative disorders including HD and PD, which supports the beneficial effects found for CB2 receptor agonists in both disorders. In conclusion, the evidence reported so far supports that those cannabinoids having antioxidant properties and/or capability to activate CB2receptors may represent promising therapeutic agents in HD and PD, thus deserving a prompt clinical evaluation.Wiley Online LibraryUniversidad Complutense de Madrid20112011-01-0120112011-01-01journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/93221reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Attribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/932212026-06-02T12:44:21Z
dc.title.none.fl_str_mv Prospects for cannabinoid therapies in basal ganglia disorders
title Prospects for cannabinoid therapies in basal ganglia disorders
spellingShingle Prospects for cannabinoid therapies in basal ganglia disorders
Fernández Ruiz, José Javier
61
Basal ganglia
Cannabinoid signalling system
Cannabinoids
CB1 receptors
CB2 receptors
Neurodegeneration
Neuroprotection
Ciencias Biomédicas
Ciencias
24 Ciencias de la Vida
title_short Prospects for cannabinoid therapies in basal ganglia disorders
title_full Prospects for cannabinoid therapies in basal ganglia disorders
title_fullStr Prospects for cannabinoid therapies in basal ganglia disorders
title_full_unstemmed Prospects for cannabinoid therapies in basal ganglia disorders
title_sort Prospects for cannabinoid therapies in basal ganglia disorders
dc.creator.none.fl_str_mv Fernández Ruiz, José Javier
Moreno Martet, Miguel
Rodríguez Cueto, Carmen Aurora
Palomo Garo, Cristina
Gómez Cañas, María
Valdeolivas, Sara
Guaza, Carmen
Romero, Julián
Guzmán Pastor, Manuel
Mechoulam, Raphael
Ramos Atance, José Antonio
author Fernández Ruiz, José Javier
author_facet Fernández Ruiz, José Javier
Moreno Martet, Miguel
Rodríguez Cueto, Carmen Aurora
Palomo Garo, Cristina
Gómez Cañas, María
Valdeolivas, Sara
Guaza, Carmen
Romero, Julián
Guzmán Pastor, Manuel
Mechoulam, Raphael
Ramos Atance, José Antonio
author_role author
author2 Moreno Martet, Miguel
Rodríguez Cueto, Carmen Aurora
Palomo Garo, Cristina
Gómez Cañas, María
Valdeolivas, Sara
Guaza, Carmen
Romero, Julián
Guzmán Pastor, Manuel
Mechoulam, Raphael
Ramos Atance, José Antonio
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv 61
Basal ganglia
Cannabinoid signalling system
Cannabinoids
CB1 receptors
CB2 receptors
Neurodegeneration
Neuroprotection
Ciencias Biomédicas
Ciencias
24 Ciencias de la Vida
topic 61
Basal ganglia
Cannabinoid signalling system
Cannabinoids
CB1 receptors
CB2 receptors
Neurodegeneration
Neuroprotection
Ciencias Biomédicas
Ciencias
24 Ciencias de la Vida
description Cannabinoids are promising medicines to slow down disease progression in neurodegenerative disorders including Parkinson's disease (PD) and Huntington's disease (HD), two of the most important disorders affecting the basal ganglia. Two pharmacological profiles have been proposed for cannabinoids being effective in these disorders. On the one hand, cannabinoids like Δ9‐tetrahydrocannabinol or cannabidiol protect nigral or striatal neurons in experimental models of both disorders, in which oxidative injury is a prominent cytotoxic mechanism. This effect could be exerted, at least in part, through mechanisms independent of CB1 and CB2 receptors and involving the control of endogenous antioxidant defences. On the other hand, the activation of CB2 receptors leads to a slower progression of neurodegeneration in both disorders. This effect would be exerted by limiting the toxicity of microglial cells for neurons and, in particular, by reducing the generation of proinflammatory factors. It is important to mention that CB2 receptors have been identified in the healthy brain, mainly in glial elements and, to a lesser extent, in certain subpopulations of neurons, and that they are dramatically up‐regulated in response to damaging stimuli, which supports the idea that the cannabinoid system behaves as an endogenous neuroprotective system. This CB2 receptor up‐regulation has been found in many neurodegenerative disorders including HD and PD, which supports the beneficial effects found for CB2 receptor agonists in both disorders. In conclusion, the evidence reported so far supports that those cannabinoids having antioxidant properties and/or capability to activate CB2receptors may represent promising therapeutic agents in HD and PD, thus deserving a prompt clinical evaluation.
publishDate 2011
dc.date.none.fl_str_mv 2011
2011-01-01
2011
2011-01-01
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/93221
url https://hdl.handle.net/20.500.14352/93221
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
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
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
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Wiley Online Library
publisher.none.fl_str_mv Wiley Online Library
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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