Cannabidiol and the Canonical WNT/β-Catenin Pathway in Glaucoma

Glaucoma is a progressive neurodegenerative disease which constitutes the main frequent cause of irreversible blindness. Recent findings have shown that oxidative stress, inflammation and glutamatergic pathway play key roles in the causes of glaucoma. Recent studies have shown a down regulation of the WNT/beta-catenin pathway in glaucoma, associated with overactivation of the GSK-3 beta signaling. WNT/beta-catenin pathway is mainly associated with oxidative stress, inflammation and glutamatergic pathway. Cannabidiol (CBD) is a non-psychotomimetic phytocannabinoid derived from Cannabis sativa plant which possesses many therapeutic properties across a range of neuropsychiatric disorders. Since few years, CBD presents an increased interest as a possible drug in anxiolytic disorders. CBD administration is associated with increase of the WNT/beta-catenin pathway and decrease of the GSK-3 beta activity. CBD has a lower affinity for CB1 but can act through other signaling in glaucoma, including the WNT/beta-catenin pathway. CBD downregulates GSK3-beta activity, an inhibitor of WNT/beta-catenin pathway. Moreover, CBD was reported to suppress pro-inflammatory signaling and neuroinflammation, oxidative stress and glutamatergic pathway. Thus, this review focuses on the potential effects of cannabidiol, as a potential therapeutic strategy, on glaucoma and some of the presumed mechanisms by which this phytocannabinoid provides its possible benefit properties through the WNT/beta-catenin pathway.

Automated summary

Glaucoma is a progressive neurodegenerative disease with oxidative stress, inflammation, and glutamatergic pathway playing key roles. CBD, a non-psychotomimetic phytocannabinoid, has shown potential therapeutic effects on glaucoma by increasing the WNT/beta-catenin pathway and reducing GSK-3 beta activity.