Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/21033
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dc.contributor.authorFernández-Ruiz, Javier
dc.contributor.authorMoro, María A
dc.contributor.authorMartínez-Orgado, José
dc.date.accessioned2019-06-28T13:09:18Z-
dc.date.available2019-06-28T13:09:18Z-
dc.date.issued2015-10
dc.identifier.citationNeurotherapeutics.2015 Oct;(12)4:793-806
dc.identifier.urihttps://hdl.handle.net/20.500.12530/21033-
dc.description.abstractCannabinoids form a singular family of plant-derived compounds (phytocannabinoids), endogenous signaling lipids (endocannabinoids), and synthetic derivatives with multiple biological effects and therapeutic applications in the central and peripheral nervous systems. One of these properties is the regulation of neuronal homeostasis and survival, which is the result of the combination of a myriad of effects addressed to preserve, rescue, repair, and/or replace neurons, and also glial cells against multiple insults that may potentially damage these cells. These effects are facilitated by the location of specific targets for the action of these compounds (e.g., cannabinoid type 1 and 2 receptors, endocannabinoid inactivating enzymes, and nonendocannabinoid targets) in key cellular substrates (e.g., neurons, glial cells, and neural progenitor cells). This potential is promising for acute and chronic neurodegenerative pathological conditions. In this review, we will collect all experimental evidence, mainly obtained at the preclinical level, supporting that different cannabinoid compounds may be neuroprotective in adult and neonatal ischemia, brain trauma, Alzheimer's disease, Parkinson's disease, Huntington's chorea, and amyotrophic lateral sclerosis. This increasing experimental evidence demands a prompt clinical validation of cannabinoid-based medicines for the treatment of all these disorders, which, at present, lack efficacious treatments for delaying/arresting disease progression, despite the fact that the few clinical trials conducted so far with these medicines have failed to demonstrate beneficial effects.
dc.language.isoeng
dc.rightsopenAccess-
dc.subjectCB1 and CB2 receptors
dc.subjectCannabinoids
dc.subjectEndocannabinoid signaling system
dc.subjectFAAH and MAGL enzymes
dc.subjectNeurodegenerative disorders
dc.subjectNeuroprotection
dc.subject.meshAnimals
dc.subject.meshBrain Injuries
dc.subject.meshCannabinoids
dc.subject.meshDisease Models, Animal
dc.subject.meshHumans
dc.subject.meshNeurodegenerative Diseases
dc.subject.meshStroke
dc.subject.meshDrug Evaluation, Preclinical
dc.titleCannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications.
dc.typeArtículo
dc.identifier.pubmedID26260390
dc.format.volume12
dc.format.page793-806
dc.identifier.e-issn1878-7479
dc.identifier.journalNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
dc.identifier.doi10.1007/s13311-015-0381-7
dc.format.number4
dc.identifier.pmcPMC4604192
dc.pubmedtypeJournal Article
dc.pubmedtypeResearch Support, Non-U.S. Gov't
dc.pubmedtypeReview
Appears in Collections:Fundaciones e Institutos de Investigación > IIS H. U. 12 de Octubre > Artículos
Fundaciones e Institutos de Investigación > IIS H. U. Clínico San Carlos > Artículos
Fundaciones e Institutos de Investigación > IIS H. U. Ramón y Cajal > Artículos

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