Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/43014
Title: Cannabinoids and neuroprotection in Basal ganglia disorders
Authors: Sagredo, Onintza
Garcia-Arencibia, Moises 
De Lago, Eva
Finetti, Simone
Decio, Alessandra
Fernández-Ruiz, Javier
UNESCO Clasification: 2302 Bioquímica
320507 Neurología
Keywords: Cannabinoids
Cannabinoid signaling system
CB1 receptors
CB2 receptors
Basal ganglia
Neurodegeneration
Neuroprotection
Parkinson’s disease
Huntington’s disease
Issue Date: 2007
Publisher: 0893-7648
Journal: Molecular Neurobiology 
Abstract: Cannabinoids have been proposed as clinically promising neuroprotective molecules, as they are capable to reduce excitotoxicity, calcium influx, and oxidative injury. They are also able to decrease inflammation by acting on glial processes that regulate neuronal survival and to restore blood supply to injured area by reducing the vasoconstriction produced by several endothelium-derived factors. Through one or more of these processes, cannabinoids may provide neuroprotection in different neurodegenerative disorders including Parkinson’s disease and Huntington’s chorea, two chronic diseases that are originated as a consequence of the degeneration of specific nuclei of basal ganglia, resulting in a deterioration of the control of movement. Both diseases have been still scarcely explored at the clinical level for a possible application of cannabinoids to delay the progressive degeneration of the basal ganglia. However, the preclinical evidence seems to be solid and promising. There are two key mechanisms involved in the neuroprotection by cannabinoids in experimental models of these two disorders: first, a cannabinoid receptor-independent mechanism aimed at producing a decrease in the oxidative injury and second, an induction/upregulation of cannabinoid CB2 receptors, mainly in reactive microglia, that is capable to regulate the influence of these glial cells on neuronal homeostasis. Considering the relevance of these preclinical data and the lack of efficient neuroprotective strategies in both disorders, we urge the development of further studies that allow that the promising expectatives generated for these molecules progress from the present preclinical evidence till a real clinical application.
URI: http://hdl.handle.net/10553/43014
ISSN: 0893-7648
DOI: 10.1007/s12035-007-0004-3
Source: Molecular Neurobiology[ISSN 0893-7648],v. 36 (1), p. 82-91
Appears in Collections:Reseña
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