The gut–brain axis in depression, anxiety, and schizophrenia: a scoping review of mechanisms, biomarkers, and therapeutic implications
Kirolos Eskandar
Abstract
Abstract Background The gut–brain axis represents a multidirectional communication system linking the gastrointestinal microbiota with neural, immune, and metabolic pathways. Emerging evidence implicates this interface in the pathophysiology of psychiatric disorders. This scoping review mapped research published between 2015 and 2025 on mechanisms, biomarkers, and therapeutic implications of the gut–brain axis in depression, anxiety, and schizophrenia. Methods A systematic search was conducted in MEDLINE, Embase, PsycINFO, Web of Science, and Scopus, supplemented with grey literature sources. Searches covered January 2015 through June 2025 and were performed between July 3rd and July 10th, 2025. Eligible studies included empirical human or animal research addressing gut–brain mechanisms, biomarkers, or microbiome-targeted interventions in the specified disorders. A total of 145 studies were included. Data were charted using a standardized extraction form and synthesized descriptively and thematically. Results Findings revealed consistent patterns of microbial dysbiosis, short-chain fatty acid disturbances, kynurenine pathway alterations, and immune activation across disorders. Biomarker studies identified candidate microbial taxa and metabolites with potential diagnostic or prognostic relevance, though reproducibility was limited. Interventional approaches—including probiotics, prebiotics, synbiotics, diet-based strategies, and fecal microbiota transplantation—showed modest benefits for depressive and anxiety symptoms but yielded mixed or preliminary findings in schizophrenia. Cross-disorder synthesis suggested both shared inflammatory-metabolic pathways and disorder-specific signatures. Conclusion The gut–brain axis provides a promising mechanistic framework and therapeutic target for major psychiatric disorders. However, methodological heterogeneity, limited causal evidence, and inconsistent biomarker validation restrict clinical translation. Future progress will depend on harmonized biomarker platforms, rigorous controlled trials, and integration of multi-omics approaches to establish clinical utility.