Gut Microbial Control of Neurotransmitters and Their Relation to Neurological Disorders: A Comprehensive Review.

The study explores the vital role of gut microbiota in regulating neurotransmitters and its subsequent effects on brain function and mental health. It aims to unravel the mechanisms by which microbial metabolites influence neurotransmitter synthesis and signaling. The ultimate goal is to identify potential therapeutic strategies targeting gut microbiota for the management and treatment of neurological disorders, such as depression, autism spectrum disorder (ASD), anxiety, and Parkinson's disease. The review synthesizes current research on the gut-brain axis, focusing on the influence of gut microbial metabolites on key neurotransmitters, including dopamine, serotonin, and gamma-aminobutyric acid (GABA). It incorporates a multidisciplinary approach, linking microbiology, neurobiology, and clinical research. Each section presents an in-depth review of scientific studies, clinical trials, and emerging therapeutic strategies. The findings highlight the intricate interplay between gut microbiota and the central nervous system. Gut microbes significantly impact the synthesis and signaling of crucial neurotransmitters, which play a pivotal role in neurological health. Evidence supports the hypothesis that modulating gut microbiota can alter neurotransmitter output and alleviate symptoms associated with neurological disorders. Notable therapeutic potentials include microbiota-targeted interventions for managing depression, ASD, anxiety, and Parkinson's disease. This comprehensive analysis underscores the critical connection between gut microbiota and neurological health. By bridging gaps between microbiology, neurobiology, and clinical practice, the study opens avenues for innovative therapeutic approaches. It provides a valuable resource for researchers, clinicians, and students, emphasizing the need for continued investigation into gut microbiota's role in neurological disorders and its therapeutic potential.