Review Volume 13, Issue 7 pp 10796—10813

Potential role of cannabidiol in Parkinson’s disease by targeting the WNT/β-catenin pathway, oxidative stress and inflammation

Alexandre Vallée1, , Jean-Noël Vallée2,3, , Yves Lecarpentier4, ,

  • 1 Department of Clinical Research and Innovation (DRCI), Foch Hospital, Suresnes 92150, France
  • 2 Centre Hospitalier Universitaire (CHU) Amiens Picardie, Université Picardie Jules Verne (UPJV), Amiens 80054, France
  • 3 Laboratoire de Mathématiques et Applications (LMA), UMR CNRS 7348, Université de Poitiers, Poitiers 86000, France
  • 4 Centre de Recherche Clinique, Grand Hôpital de l’Est Francilien (GHEF), Meaux 77100, France

Received: November 20, 2020       Accepted: March 26, 2021       Published: April 13, 2021
How to Cite

Copyright: © 2021 Vallée et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Parkinson’s disease (PD) is a major neurodegenerative disease (ND), presenting a progressive degeneration of the nervous system characterized by a loss of dopamine in the substantia nigra pars compacta. Recent findings have shown that oxidative stress and inflammation play key roles in the development of PD. However, therapies remain uncertain and research for new treatment is of the utmost importance. This review focuses on the potential effects of using cannabidiol (CBD) as a potential therapeutic strategy for the treatment of PD and on some of the presumed mechanisms by which CBD provides its beneficial properties. CBD medication downregulates GSK-3β, the main inhibitor of the WNT/β-catenin pathway. Activation of the WNT/β-catenin could be associated with the control of oxidative stress and inflammation. Future prospective clinical trials should focus on CBD and its multiple interactions in the treatment of PD.


GSK-3β: Glycogen synthase kinase-3β; LRP 5/6: Low-density lipoprotein receptor-related protein 5/6; NF-κB: nuclear factor kappaB; PPARγ: Peroxisome proliferator-activated receptor gamma; PI3K-Akt: Phosphatidylinositol 3-kinase-protein kinase B; TCF/LEF: T-cell factor/lymphoid enhancer factor; TNF-α: tumor necrosis factor alpha; PD: Parkinson’s disease.