Drug-resistant epilepsy affects a significant portion of people with epilepsy and is often linked to underlying processes such as chronic neuroinflammation, oxidative stress, and progressive neuronal damage. This review explores the potential role of cannabigerol (CBG), a non-intoxicating cannabinoid, by examining how it interacts with biological systems involved in brain health. Rather than focusing on direct seizure control, the study looks at how CBG may influence the underlying mechanisms that contribute to disease progression, including immune signaling, neuronal survival, and brain plasticity.

The review highlights that CBG interacts with multiple molecular targets, including cannabinoid receptors, TRP channels, and nuclear receptors such as PPARγ. Through these interactions, preclinical studies suggest that CBG may help reduce neuroinflammation, limit oxidative damage, and support neuronal survival and connectivity. Evidence from laboratory and animal models shows that CBG can influence pathways involved in cell survival and neuroprotection, potentially helping stabilize brain function under stress or injury conditions.

However, the authors emphasize that current evidence is still preclinical and hypothesis-generating, meaning there is not yet direct clinical proof that CBG can treat epilepsy or reduce seizures in humans. The review serves as a framework for future research, suggesting that targeting inflammation and neurodegeneration with compounds like CBG may be a promising direction for developing new approaches to drug-resistant epilepsy. Further clinical studies are needed to confirm safety, effectiveness, and real-world applications.

Source:
Patricio-Martínez A, et al. Elucidating the putative role of cannabigerol: a hypothesis-generating review of neuroinflammatory and neuroprotective mechanisms with implications for drug-resistant epilepsy. National Library of Medicine (NIH):
https://pmc.ncbi.nlm.nih.gov/articles/PMC13033654/