Neurokinin B, Neurotensin, and Cannabinoid Receptor Antagonists and Parkinson Disease

Mesnage, Valérie; Houeto, J. L.; Bonnet, Anne‐Marie; Clavier, I; Arnulf, Isabelle; Cattelin, F; Fur, G. Le; Damier, P.; Welter, Marc; Agid, Yves

doi:10.1097/00002826-200405000-00003

Cited by 126 publications

(87 citation statements)

References 9 publications

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“…Notwithstanding the above, studies using SR141716 in rat and primate models of PD or LID (Meschler et al, 2001;van der Stelt et al, 2005) provided conflicting results. Rimonabant treatment also failed to influence dyskinesia in the first small-scale, randomized, double-blind, placebo-controlled human study (Mesnage et al, 2004). However, the dose used in this human study was approximately 10-fold lower (0.3 mg/kg versus.…”

mentioning

confidence: 79%

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

2006

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confidence: 79%

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

2006

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“…Finally, an open-Blabel^study of smoked marijuana in 22 Israeli patients showed improvement in the number of dyskinesias observed after dopa challenge, 30 min after smoking the cigarette [19]. In an interesting twist, a single dose of the CB 1 R antagonist rimonabant (SR141716) was found to have no effect on motor symptoms, or induced dyskinesias in 8 patients [20].…”

Section: Dyskinesias From Levodopa (In Advanced Pd)mentioning

confidence: 95%

Cannabis in the Treatment of Dystonia, Dyskinesias, and Tics

Koppel

2015

Neurotherapeutics

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Cannabis has been used for many medicinal purposes, including management of spasms, dystonia, and dyskinesias, with variable success. Its use for tetanus was described in the second century BCE, but the literature continues to include more case reports and surveys of its beneficial effects in managing symptoms of hyperkinetic movement disorders than randomized controlled trials, making evidence-based recommendations difficult. This paper reviews clinical research using various formulations of cannabis (botanical products, oral preparations containing Δ 9 -tetrahydrocannabinol and/or cannabidiol) and currently available preparations in the USA (nabilone and dronabinol). This has been expanded from a recent systematic review of cannabis use in several neurologic conditions to include case reports and case series and results of anonymous surveys of patients using cannabis outside of medical settings, with the original evidence classifications marked for those papers that followed research protocols. Despite overlap in some patients, dyskinesias will be treated separately from dystonia and chorea; benefit was not established beyond individual patients for these conditions. Tics, usually due to Tourettes, did respond to cannabis preparations. Side effects reported in the trials will be reviewed but those due to recreational use, including the dystonia that can be secondary to synthetic marijuana preparations, are outside the scope of this paper.

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“…Lastly, clinical studies with cannabinoids in patients with PD are still limited, with most of them addressing only the relief of specific symptoms, for example bradykinesia [123], tremor [124], and levodopa-induced dyskinesia [125]. No clinical data exist in relation to the neuroprotective effects of cannabinoids.…”

Section: Cannabinoids and Chronic Neurodegenerative Disorders: II Pdmentioning

confidence: 99%

Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications

2015

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Cannabinoids form a singular family of plantderived 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.

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Neurokinin B, Neurotensin, and Cannabinoid Receptor Antagonists and Parkinson Disease

Cited by 126 publications

References 9 publications

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

Cannabis in the Treatment of Dystonia, Dyskinesias, and Tics

Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications

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