Abstract
Unlike other neuroinflammatory disorders, like Parkinsons disease, Huntingtons disease and multiple sclerosis, little is still known of the role of the endocannabinoid system in Alzheimers disease (AD). This is partly due to the poor availability of animal models that are really relevant to the human disease, and to the complexity of AD as compared to other neurological states. Nevertheless, the available data indicate that endocannabinoids are likely to play in this disorder a role similar to that suggested in other neurodegenerative diseases, that is, to represent an endogenous adaptive response aimed at counteracting both the neurochemical and inflammatory consequences of β-amyloid-induced tau protein hyperactivity, possibly the most important underlying cause of AD. Furthermore, plant and synthetic cannabinoids, and particularly the non-psychotropic cannabidiol, might also exert other, non-cannabinoid receptor-mediated protective effects, including, but not limited to, anti-oxidant actions. There is evidence, from in vivo studies on β-amyloid-induced neurotoxicity, also for a possible causative role of endocannabinoids in the impairment in memory retention, which is typical of AD. This might open the way to the use of cannabinoid receptor antagonists as therapeutic drugs for the treatment of cognitive deficits in the more advanced phases of this disorder. The scant, but nevertheless important literature on the regulation and role of the endocannabinoid system in AD, and on the potential treatment of this disorder with cannabinoids and endocannabinoid-based drugs, are discussed in this mini-review.
Keywords: Endocannabinoid System, Alzheimer's Disease, Hypotheses, neuroinflammatory disorders, Parkinson's disease, non-psychotropic cannabidiol, anti-oxidant, drugs
Current Pharmaceutical Design
Title: The Role of the Endocannabinoid System in Alzheimers Disease: Facts and Hypotheses
Volume: 14 Issue: 23
Author(s): Tiziana Bisogno and Vincenzo Di Marzo
Affiliation:
Keywords: Endocannabinoid System, Alzheimer's Disease, Hypotheses, neuroinflammatory disorders, Parkinson's disease, non-psychotropic cannabidiol, anti-oxidant, drugs
Abstract: Unlike other neuroinflammatory disorders, like Parkinsons disease, Huntingtons disease and multiple sclerosis, little is still known of the role of the endocannabinoid system in Alzheimers disease (AD). This is partly due to the poor availability of animal models that are really relevant to the human disease, and to the complexity of AD as compared to other neurological states. Nevertheless, the available data indicate that endocannabinoids are likely to play in this disorder a role similar to that suggested in other neurodegenerative diseases, that is, to represent an endogenous adaptive response aimed at counteracting both the neurochemical and inflammatory consequences of β-amyloid-induced tau protein hyperactivity, possibly the most important underlying cause of AD. Furthermore, plant and synthetic cannabinoids, and particularly the non-psychotropic cannabidiol, might also exert other, non-cannabinoid receptor-mediated protective effects, including, but not limited to, anti-oxidant actions. There is evidence, from in vivo studies on β-amyloid-induced neurotoxicity, also for a possible causative role of endocannabinoids in the impairment in memory retention, which is typical of AD. This might open the way to the use of cannabinoid receptor antagonists as therapeutic drugs for the treatment of cognitive deficits in the more advanced phases of this disorder. The scant, but nevertheless important literature on the regulation and role of the endocannabinoid system in AD, and on the potential treatment of this disorder with cannabinoids and endocannabinoid-based drugs, are discussed in this mini-review.
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Cite this article as:
Bisogno Tiziana and Di Marzo Vincenzo, The Role of the Endocannabinoid System in Alzheimers Disease: Facts and Hypotheses, Current Pharmaceutical Design 2008; 14 (23) . https://dx.doi.org/10.2174/138161208785740027
DOI https://dx.doi.org/10.2174/138161208785740027 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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