The interaction between the gut microbiota and the central nervous system has been recognized as a significant mechanism in the pathophysiology of depression and stress; research identifying specific microbial patterns associated with these disorders is summarized in this review, highlighting dysbiotic shifts that exacerbate neuroinflammation, dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, and neurotransmitter imbalances. Microbiota compositions typically exhibit decreased diversity in stress-induced states, such as prolonged psychological stress or exposure to environmental stressors. Both proinflammatory taxa, such as Proteobacteria, overgrow, while beneficial genera, including Lactobacillus and Bifidobacterium, are depleted. These changes are linked to increased cortisol levels, compromised intestinal barrier integrity, leaky gut, and ensuing systemic inflammation that penetrates the blood-brain barrier and promotes depressive and anxiety-related traits. Reduced short-chain fatty acid (SCFA)-producing bacteria and decreased alpha-diversity indices are two recurring patterns observed in metagenomic analyses of individuals with clinical depression. To sustain neuroplastic deficits in areas such as the hippocampus and prefrontal cortex, these microbial imbalances mechanistically interfere with serotonin synthesis, gamma-aminobutyric acid (GABA) modulation, and the expression of brain-derived neurotrophic factor (BDNF). Probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary interventions are among the approaches that target microbiota restoration and show therapeutic promise in reducing symptoms. In managing stress and depression, this story highlights microbiota patterns as modifiable processes, rather than merely serving as biomarkers. The goal of this review is to examine the impact of the microbiota on depressive disorders and the underlying mechanisms that may provide novel therapeutic approaches.
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Khazaei et al. (Thu,) studied this question.
www.synapsesocial.com/papers/69a75dcfc6e9836116a280ff — DOI: https://doi.org/10.1007/s44187-026-00846-8
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