Pot for Parkinson ‘s? The Scientific Evidence Is Compelling

Pot-for-Parkinson-The-Scientific-Evidence-Is-CompellingCould the very plant that for decades was accused of “frying” users’ brains be far superior to pharmaceuticals in treating the “incurable” neurodegenerative condition known as Parkinson’s disease?

Despite the political controversy surrounding medical marijuana use in the country, research has begun to emerge showing that a component of this plant known as cannabidiol (CBD), and which does not have the controversial psychoactive properties associated with tetrahydrocannabinol (THC), may have a wide range of therapeutic applications, including treating conditions that are refractory to conventional drug-based approaches.

One such condition is Parkinson’s disease, to which there is, at present, no effective conventional treatment.

In fact, the primary treatment involves dopamine increasing drugs that also increase a neurotoxic metabolite known as with 6-hydroxy-dopamine, and which therefore can actually accelerate the progression of the disease.

This is why natural alternatives that are safe, effective, and backed up by scientific evidence, are so needed today.

Thankfully, preclinical research on cannabidiol has already revealed some promising results, including two studies in animal models of Parkinson’s disease (PD) assessing its neuroprotective properties:

“In the first one, Lastres-Becker et al. (2005) showed that the administration of CBD counteracted neurodegeneration caused by the injection of 6-hydroxy-dopamine in the medial prosencephalic bundle, an effect that could be related to the modulation of glial cells and to antioxidant effects (Lastres- Becker et al., 2005). In the next year, Garcia-Arencibia et al. (2007) tested many cannabinoid compounds following the lesion of dopaminergic neurons in the substantia nigra with 6-hydroxy-dopamine and found that the acute administration of CBD seemed to have a neuroprotective action; nonetheless, the administration of CBD one week after the lesion had no significant effects (Garcia-Arencibia et al., 2007). This study also pointed to a possible antioxidant effect with the upregulation of  mRNA of the enzyme Cu-Zn-superoxide dismutase following the administration of CBD.” [1]

In addition to these animal studies, the following three human clinical trials have been conducted to evaluate cannabidiol’s neuroprotective effects.

  • A 2006 study published in Biological Psychology titled, “Dorsolateral Prefrontal Cortex N-Acetylaspartate/Total Creatine (NAA/tCr) Loss in Male Recreational Cannabis Users,” investigated the N-acetylaspartate to creatine ratios (NAA/Cr) in the brain of regular cannabis users through magnetic resonance spectroscopy (H1-MRS) to assess the neurotoxic and neuroprotective effects of cannabinoids present in the drug and found a strong positive correlation between CBD and NAA/Cr in the globus pallidus and putamen.[2] According to the study, “the globus pallidum is the region with the highest amount of CB1-receptors in the brain and the target of neurostimulation in patients with Parkinson’s disease, who developed a strong tremor. Our MRSI results support a positive effect of CBD on the putamen/globus pallidum region in cannabis use. Therefore, it may be promising to test a possible influence of the nonpsychotropic CBD in the onset of Parkinson’s disease.”
  • A 2009 study published in the Journal of Psychopharmacology titled, “Cannabidiol for the treatment of psychosis in Parkinson’s disease,”[3] assessed the therapeutic use and neuroprotective effect of CBD in PD patients. The open label study was conducted with six patients with PD-related psychosis. They were administered CBD at doses ranging from 150 mg in the first week to 400 mg in the fourth and last week of treatment (doses were adjusted to optimize the clinical response). The study reported significant improvements in psychosis as well as in the total scores of a scale that measures general symptoms of PD (Unified Parkinson’s disease rating scale – UPDRS)
  • A 2014 study published in the Journal of Psychopharmacology titled, “Effects of cannabidiol in the treatment of patients with Parkinson’s disease: an exploratory double-blind trial,” evaluated the effects of cannabidiol in Parkinson’s disease patients, dividing 21 patients into 3 groups of 7 receiving either placebo, cannabidiol (CBD) 75 mg/day or CBD 300 mg/day. Increases in well-being and quality of life were observed in the 300 mg/day groups versus the placebo groups. The researchers hypothesized that these improvements may have been due to cannabidiol’s “anxiolytic,” “antidepressant,” “anti-psychotic,” and “sedative” properties.

These results, taken together with the results from the animal models of PD, indicate that CBD may provide a drug alternative in PD patients. Additionally, a new study published in Toxicology In Vitro titled,”The neuroprotection of cannabidiol against MPP+-induced toxicity in PC12 cells involves trkA receptors, upregulation of axonal and synaptic proteins, neuritogenesis, and might be relevant to Parkinson’s disease,” makes the case for using cannabidiol in PD even more compelling by helping to illuminate some of the molecular mechanisms beneath its benefits.

The study found that cannabidiol protects against the neurotoxin known as MPP(+), which is widely believed to be responsible for the damage to the dopamine-producing cells in the substania nigra of Parkison’s patients, by preventing neuronal cell death and inducing neuritogenesis (a neuro-regenerative process for repairing damaged neurons). This mechanism was found to be independent of the neural growth factor (NGF) pathway, even though it involves NGF receptors. Cannabidiol was also found to increase the expression of axonal and synaptic proteins. The study concluded that CBD’s neuroprotective properties might be of benefit to Parkinson’s disease patients.


References

[1] Chagas MH, et al. J Psychopharmacol. 2014 Nov;28(11):1088-98. doi: 10.1177/0269881114550355. Epub 2014 Sep 18. Effects of cannabidiol in the treatment of patients with Parkinson’s disease: an exploratory double-blind trial.

[2] Hermann D, Sartorius A, Welzel H, et al. (2007) Dorsolateral prefrontal cortex N-acetylaspartate/total creatine (NAA/tCr) loss in male recreational cannabis users. Biol Psychiatry 61: 1281–1289.

[3] Zuardi AW, Crippa JA, Hallak JE, et al. (2009) Cannabidiol for the treatment of psychosis in Parkinson’s disease. J Psychopharmacol 23:979–983.

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