Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/43007
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dc.contributor.authorGarcía-Arencibia, Moisésen_US
dc.contributor.authorGarcía, Concepciónen_US
dc.contributor.authorFernández-Ruiz, Javieren_US
dc.contributor.otherGarcia-Arencibia, Moises-
dc.contributor.otherGarcia, Concepcion-
dc.contributor.otherGarcia-Arencibia, Moises-
dc.date.accessioned2018-11-21T12:03:57Z-
dc.date.available2018-11-21T12:03:57Z-
dc.date.issued2009en_US
dc.identifier.issn1871-5273en_US
dc.identifier.urihttp://hdl.handle.net/10553/43007-
dc.description.abstractCannabinoid-based medicines have been proposed as clinically promising therapies in Parkinsons disease (PD), given the prominent modulatory function played by the cannabinoid signaling system in the basal ganglia. Supporting this pharmacological potential, the cannabinoid signaling system experiences a biphasic pattern of changes during the progression of PD. Thus, early and presymptomatic stages, characterized by neuronal malfunctioning but little evidence of neuronal death, are associated with desensitization/downregulation of CB1 receptors. It was proposed that these losses may be part of the pathogenesis itself, since they can aggravate different cytotoxic insults which are controlled in part by cannabinoid signals, mainly excitotoxicity but also oxidative stress and glial activation. By contrast, intermediate and, in particular, advanced stages of parkinsonism characterized by a profound nigral degeneration and occurrence of major parkinsonian symptoms (e.g. bradykinesia), are associated with upregulatory responses of CB1 receptors, possibly CB2 receptors too, and the endocannabinoid ligands for both receptor types. This would explain the motor inhibition typical of this disease and the potential proposed for CB1 receptor antagonists in attenuating the bradykinesia typical of PD. In addition, certain cannabinoid agonists have been proposed to serve as neuroprotective molecules in PD, given their well-demonstrated capability to reduce excitotoxicity, calcium influx, glial activation and, in particular, oxidative injury that cooperatively contribute to the degeneration of nigral neurons. However, the potential of cannabinoid-based medicines in PD have been still scarcely studied at the clinical level despite the existence of solid and promising preclinical evidence. Considering the relevance of these preclinical data, the need for finding treatments for motor symptoms that may be alternative to classic dopaminergic replacement therapy, and the lack of efficient neuroprotective strategies in PD, we believe it is of major interest to develop further studies that allow the promising expectations generated for these molecules to progress from the present preclinical evidence towards a real clinical application.en_US
dc.languageengen_US
dc.publisher1871-5273-
dc.relation.ispartofCNS and Neurological Disorders - Drug Targetsen_US
dc.sourceCNS and Neurological Disorders - Drug Targets [ISSN 1871-5273], v. 8, p. 432-439en_US
dc.subject320507 Neurologíaen_US
dc.subject.otherCannabinoidsen_US
dc.subject.otherCannabinoid signaling systemen_US
dc.subject.otherCB1 receptorsen_US
dc.subject.otherCB2 receptorsen_US
dc.subject.otherBasal gangliaen_US
dc.subject.otherMotor inhibitionen_US
dc.subject.otherNeurodegenerationen_US
dc.subject.otherNeuroprotectionen_US
dc.subject.otherParkinson's diseaseen_US
dc.titleCannabinoids and Parkinson's Diseaseen_US
dc.typeinfo:eu-repo/semantics/articlees
dc.typeArticlees
dc.identifier.doi10.2174/187152709789824642-
dc.identifier.doiWOS:000272738000004-
dc.identifier.scopus75849118409-
dc.identifier.isi000272738000004-
dcterms.isPartOfCns & Neurological Disorders-Drug Targets-
dcterms.sourceCns & Neurological Disorders-Drug Targets[ISSN 1871-5273],v. 8 (6), p. 432-439-
dc.contributor.authorscopusid15821889300-
dc.contributor.authorscopusid7401486282-
dc.contributor.authorscopusid7006533053-
dc.description.lastpage439-
dc.description.firstpage432-
dc.relation.volume8-
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000272738000004-
dc.contributor.daisngid1760567-
dc.contributor.daisngid3366447-
dc.contributor.daisngid180726-
dc.identifier.investigatorRIDK-9920-2013-
dc.identifier.investigatorRIDH-9138-2015-
dc.identifier.investigatorRIDB-5538-2012-
dc.identifier.ulpgces
dc.description.jcr3,571
dc.description.jcrqQ1
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.orcid0000-0002-1618-4487-
crisitem.author.fullNameGarcía Arencibia, Moisés-
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