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Introduction: The endocannabinoid system (ECS) plays a critical role in the modulation of various neurotransmitters, including dopamine, glutamate, and γ-aminobutyric acid, through its lipid-based endogenous mediators such as anandamide (AEA) and 2-arachidonoylglycerol (2-AG). The dualistic nature of its interaction—mediating both neuroprotective and potentially psychotropic effects—makes the ECS a compelling subject of study in psychiatric disorders.
Objective: This study aims to elucidate the role of the ECS and low-grade inflammation in psychiatric disorders within the spectrum of psychosis, including schizophrenia, schizoaffective disorders, and bipolar disorders. Specifically, we focus on the potential diagnostic and therapeutic implications of ECS biomarkers and inflammatory profiles in these conditions.
Methods: We conducted a cross-sectional analysis involving 116 individuals categorized into groups based on their diagnosis: schizophrenia, schizoaffective disorder, bipolar disorder, and controls. Biomarkers measured included AEA and 2-AG levels, as well as inflammatory markers IL-1ß, TNFα, IL-6, and C-reactive protein (CRP). Statistical analysis involved the Kruskal-Wallis test to compare differences across groups, followed by Spearman’s rank correlation to examine the associations between these biomarkers and clinical parameters. Blood serum concentrations of interleukin 1 beta (IL-1- beta), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha) and C-reactive protein (CRP), were determined using commercial human-specific enzyme-linked immunosorbent assay (ELISA) kits. Endocannabinoids, AEA and 2-AG levels, were measured using competitive ELISA according to the manufacturer’s instructions.
Results: Our findings indicated significant variations in AEA and 2-AG levels across different psychiatric conditions. The study has demonstrated that both patients with schizophrenia compared to the control group (125.04 ng/ml vs. 88.79 ng/ml, p=0.014) and those with schizoaffective disorder compared to the control group (145.90 ng/ml vs. 88.79 ng/ml, p=0.001) showed elevated AEA levels suggesting its potential role as a biomarker for psychosis. The analysis also revealed significant correlations between ECS components and inflammatory markers, particularly higher AEA levels associated with reduced inflammatory profiles in schizoaffective patients (p=-0,68). These results suggest an intricate link between the ECS, inflammatory processes, and the pathophysiology of psychotic disorders.
Discussion: The significant correlations between endocannabinoid levels and low-grade inflammation highlight the ECS's potential as a target for therapeutic intervention. The anti-inflammatory properties of cannabinoids, particularly cannabidiol, may offer new avenues for treating psychosis with fewer side effects compared to traditional antipsychotics. Moreover, the interaction between dietary lipids, ECS activity, and inflammation underscores the potential for dietary interventions to modify disease outcomes in psychiatric patients.
Conclusion: The study emphasizes the significant role of the ECS and inflammatory processes in psychiatric disorders across the psychotic spectrum. The results support further research into the ECS as a biomarker for psychosis and a target for novel therapeutic strategies, emphasizing the need for integrated approaches that consider both neurochemical and inflammatory aspects of psychiatric illnesses. Future studies should explore the longitudinal impact of ECS modulation on disease progression and treatment response in these disorders.
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