Investigating Cannabidiol's potential as a supplementary treatment for schizophrenia: A narrative review.

Schizophrenia presents a complex mental health challenge, often inadequately addressed by existing antipsychotic treatments, leading to persistent symptoms and adverse effects. Hence, developing alternative therapeutic approaches is crucial. Cannabidiol (CBD), a nonpsychoactive compound in Cannabis sativa, has been extensively explored for its therapeutic potential in treating psychiatric disorders, including schizophrenia. CBD exhibits antipsychotic, anxiolytic, and neuroprotective effects. However, distinguishing the individual effects of CBD and THC remains challenging. Therefore, this review aims to critically analyze the potential role of CBD as an adjunctive therapy in schizophrenia treatment. The therapeutic action of CBD may involve activating the 5-hydroxytryptamine 1A receptors and suppressing the G-protein-coupled receptor 55, thereby affecting various neurotransmitter systems. Additionally, the anti-inflammatory and antioxidative effects of CBD may contribute to alleviating neuroinflammation linked to schizophrenia. Compared to typical antipsychotics, CBD demonstrates a lower incidence of side effects and it exhibited favorable tolerability in clinical trials. A 2012 clinical trial demonstrated the efficacy of CBD in reducing both positive and negative symptoms of schizophrenia, presenting a safer profile than that of traditional antipsychotics. However, further research is needed to fully establish the safety and efficacy of CBD as an adjunctive treatment. Future research directions encompass exploring detailed antipsychotic mechanisms, long-term safety profiles, interactions with current antipsychotics, optimal dosing, and patient-specific factors such as genetic predispositions. Despite these research needs, the potential of CBD to enhance the quality of life and symptom management positions it as a promising candidate for innovative schizophrenia treatment approaches.

The Modulatory Effect of Metformin on Ethanol-Induced Anxiety, Redox Imbalance, and Extracellular Matrix Levels in the Brains of Wistar Rats.

The study investigated the potential neuroprotective effects of metformin (MET) on alcohol-induced neurotoxicity in adult Wistar rats. The animals were randomized in four groups (n = 10): control, alcohol (ALC), ALC + MET, and MET. ALC (2 g/kg b.w.) and MET (200 mg/kg b.w.) were orally administered for 21 days, once daily. For the ALC + MET group, MET was administered 2 h after ALC treatment. On day 22, the open field test (OFT) and elevated plus maze (EPM) were performed. MET improved global activity and increased the time spent in unprotected open arms, decreased oxidative stress, both in the frontal lobe and in the hippocampus, and increased neuroglobin expression in the frontal cortex. Histopathologically, an increased neurosecretory activity in the frontal cortex in the ALC + MET group was noticed. Thus, our findings suggest that metformin has antioxidant and anxiolytic effects and may partially reverse the neurotoxic effects induced by ethanol.