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These include pain in the shoulder or neck area or in the back, as well as a slowing down and decrease in movement. In addition, there is a rest tremor that begins on one side. In the course of the disease, the gait pattern changes. Those affected bend forward and take only small, short steps.

Effects of cannabidiol in the treatment of patients with Parkinson's disease: An exploratory double-blind trial - Marcos Hortes N Chagas, Antonio W Zuardi, Vitor Tumas, Márcio Alexandre Pena-Pereira, Emmanuelle T Sobreira, Mateus

Later, affect lability, apathy, anxiety disorders and dementia may develop. These non-motor symptoms should not be underestimated, as they often severely limit the patient’s quality of life. Source: Photo by Hugo Delauney on Unsplash .

Sharon Zhang, BSN, RN, Seattle University College of Nursing, Seattle, WA.

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This work is a literature review, presenting the current state of the use of cannabinoids on neurodegenerative diseases. The emphasis is on Parkinson’s (PD) and Alzheimer’s (AD) diseases, the two most prevalent neurological diseases. The review goes from Cannabis sativa and its hundreds of bioactive compounds to Δ9-tetrahydrocannabinol (THC) and mainly cannabidiol (CBD) and their interactions with the endocannabinoid receptors (CB1 and CB2).

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Although THC is the main psychoactive component of C. sativa, and it may induce transient psychosis-like symptoms, growing evidence suggests that CBD may have protective effects against the psychotomimetic effects of THC and therapeutic properties. Furthermore, a great number of recent works on the neuroprotective and anti-inflammatory CBD effects and its molecular targets are also reviewed.

Although the data on preclinical assays are more convincing, the same is not true with the clinical data. Despite the consensus among researchers on the potential of CBD as a neuroprotective agent, larger and well-designed randomized clinical trials will be necessary to gather conclusive results concerning the use of CBD as a therapeutic strategy for the treatment of diseases such as PD and AD.

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Published by S. Karger AG, Basel Cannabis sativa L. (fam. Cannabaceae) is a medicinal plant cultivated throughout millennia, for agricultural, industrial, and medicinal purposes, among others. Over the years, it became a controversial plant, due to its psychoactive effects. Since then, C. sativa has moved back and forth from the category of herbal medicine to an illicit drug and again to a medicinal product [1].

sativa and more than 100 phytocannabinoids among which are Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD). These phytocannabinoids work by binding to cannabinoid receptors (CB1 and CB2), as well as to other receptor systems [2]. THC is the main psychotropic constituent of C. sativa and a CB1 and CB2 receptor partial agonist.

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CBD displays unexpectedly high potency as an antagonist of CB1/CB2 receptor agonists [3]. CB1 receptors are present at very high levels in the brain and mediate many of the psychoactive effects of cannabinoids, while CB2 receptors have a more restricted distribution, being present mainly in the peripheral system, i. e., immune cells, and in a few neurons.

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Due to their expression and localization in the CNS, the CB1 receptor, endocannabinoids, and the enzymes involved in the synthesis and degradation of these endocannabinoids are implicated in multiple pathophysiological events, ranging from memory deficits to neurodegenerative diseases [5]. Furthermore, the phytocannabinoids and terpenoids present in C. sativa may act in concert to elicit therapeutic effects.

Evidence has raised the possibility that CBD can act as a negative allosteric modulator of CB1. Results from computational methods offer a possible explanation of how CBD can directly modulate the effects of THC on CB1 receptors [7]. Besides, several studies have described CBD as a multitarget molecule, acting as an adaptogen and as a modulator, in different ways, depending on the type and location of disequilibrium, both in the brain and in the body, mainly interacting with specific CB1 and CB2 receptor proteins [8, 9].

Despite animal studies suggesting a low oral bioavailability, the literature on humans is not sufficient. According to Millar and coworkers, 2018 [10], of the 792 articles retrieved, only 24 included pharmacokinetic parameters in humans. The half-life of CBD was reported between 1. 4 and 10. 9 h after oromucosal spray, 2–5 days after chronic oral administration, 24 h after i.

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The authors conclude that understanding properties, such as bioavailability and half-life, is critical to future therapeutic success. CBD has received great scientific interest, due to its medical applications. This compound showed efficacy as an anti-seizure, antipsychotic, neuroprotective, antidepressant, and anxiolytic. The neuroprotective activity appears linked to its excellent anti-inflammatory and antioxidant properties [11].

sativa, with an emphasis on CBD as a therapeutic strategy for the management of neurodegenerative diseases such as Parkinson’s (PD) and Alzheimer’s diseases (AD). Neurodegenerative diseases represent one of the main causes of death in industrialized countries and are characterized by a loss of neurons, in particular regions of the central nervous system [12].