A new animal trial published in Frontiers in Neuroscience suggests cannabinoids may elicit significant neuroprotection that could inhibit Parkinson’s disease. Researchers from the United Arab Emirates University used six to seven month old rats that had been induced with Parkinson’s, and in one group, administered 50 mg/kg of β-caryophyllene (BCP) daily for four weeks before examining their brains. They found that BCP effectively upregulated the expression of CB2 receptors in comparison with the control group, and produced anti-inflammatory and antioxidant effects that help to prevent neurodegeneration. They found that their activation reduced the loss of dopamine-producing neurons and the oxidative stress biomarker malondialdehyde, thus preventing a drop in the antioxidant glutathione. Additionally, CB2 activation augmented the antioxidant enzymes superoxide dismutase and catalase, which alleviated the Parkinson’s disease-induced glial cell activation in the striatum.
Researchers concluded, “Taken together, the abrogation of the protective effects… demonstrates the CB2 receptor-dependent mechanism of BCP and the findings can be extrapolated to the neuroprotective properties of CB2 agonism in PD.” These results support the findings of previous studies that have found cannabinoids offer neuroprotection that could benefit Parkinson’s disease. The researchers explain, “In recent years, the cannabinoid receptors, specifically activating CB2 receptors, appear to represent a novel therapeutic target for neurodegenerative diseases, including [Parkinson’s disease], because of their role in counteracting oxidative stress and inflammation… The CB2 receptors have recently emerged as a potential anti-inflammatory target, to break the self-sustaining cycle of neuroinflammation and preserve neuronal homeostasis, and survival in neurodegenerative disorders.”