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[Correlation Between Emotional-Affective Disorders and Gut Microbiota Composition in Patients with Parkinson’s Disease].
BACKGROUND: Despite the efforts of scientific community the data available on the correlation between emotional-affective symptoms of Parkinson’s disease and changes in microbiome is still scarce. Deeper studies of nonmotor symptoms evident in premotor stages of the disease and the reciprocal influence of microbiota may help to understand the etiology and pathogenesis of PD neurodegeneration better. AIM OF THE STUDY: Discover the relations between emotional-affective disorders prevalent in PD population and changes in gut microbiota composition. METHODS: 51 patient diagnosed with PD participated in the study. Every participant’s emotional-affective state was examined using Beck’s Depression Inventory (BDI) and Hospital Anxiety and Depression Scale (HADS). Taxonomic richness of microbiome was studied using 16S ribosomal RNA gene sequencing, bioinformatics, and statistical analysis. RESULTS: Anxiety and depression are prevalent affective disorders in patients with PD. In our study, most of the subjects demonstrated certain anxiety and depression. Taxonomic diversity of gut microbiota in BP was increasing with the increase in anxiety levels, reaching the maximum in the group with subclinical anxiety, and decreasing in the group with clinically significant anxiety disorder. At the species level, patients with clinically significant anxiety had higher abundance of Clostridium clariflavum compared to the anxiety-free patients. Patients with moderate depression were characterized by the higher prevalence of Christensenella minuta, Clostridium disporicum, and Oscillibacter valericigenes compared to subjects without depression or with mild depression. CONCLUSION: The data we received in our study allow better understanding of PD pathogenesis.
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Associations between specific dietary patterns, gut microbiome composition, and incident subthreshold depression in Chinese young adults.
INTRODUCTION: The interplay between influential factors and the incidence of subthreshold depression (SD) in young adults remains poorly understood. OBJECTIVES: This study sought to understand the dietary habits, gut microbiota composition, etc. among individuals with SD in young adults and to investigate their association with SD occurrence. METHODS: Employing a cross-sectional approach, 178 individuals with SD, aged 18-32 years, were matched with 114 healthy counterparts. SD status was evaluated using the Zung Self-rating Depression Scale (SDS), Zung Self-rating Anxiety Scale (SAS), Beck Depression Inventory 2nd version (BDI-II), the 17-item Hamilton Rating Scales of Depression (HAMD-17), and Pittsburgh Sleep Quality Index (PSQI). Metagenomic sequencing was utilized to identify fecal microbial profiles. Dietary patterns were discerned via factor analysis of a 25-item food frequency questionnaire (FFQ). Logistic regression analysis and mediation analysis were performed to explore the potential links between gut microbiota, dietary patterns, and incident SD. RESULTS: Data on dietary habits were available for 292 participants (mean [SD] age, 22.1 [2.9] years; 216 [73.9 %] female). Logistic regression analysis revealed that dietary patterns Ⅰ (odds ratio [OR], 0.34; 95 % CI, 0.15-0.75) and IV (OR, 0.39; 95 % CI, 0.17-0.86 and OR, 0.39; 95 % CI, 0.18-0.84) were associated with reduced risk of SD. Distinct microbial profiles were observed in young adults with SD, marked by increased microbial diversity and taxonomic alterations. Moreover, mediation analysis suggested Veillonella atypica as a potential mediator linking SDS or BDI-II scores with a healthy dietary pattern rich in bean products, coarse grains, nuts, fruits, mushrooms, and potatoes (β = 0.25, 95 % CI: 0.02-0.78 and β = 0.18, 95 % CI: 0.01-0.54). CONCLUSIONS: Our findings highlight the complex interplay between dietary patterns, gut microbiota, and the risk of developing SD in young adults, underscoring the potential for dietary interventions and microbiome modulation in mental health promotion.
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The gut-brain axis in depression: Are multi-omics showing the way?
It is time for a paradigm shift in psychiatry. The need for biologically based models to understand clinical heterogeneity is gaining momentum. Integrating the microbiome into biomarker discovery provides an accessible, biological approach to generate clinically relevant biomarkers that consider the host and the environment in a comprehensive way.
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A Gpr35-tuned gut microbe-brain metabolic axis regulates depressive-like behavior.
Gene-environment interactions shape behavior and susceptibility to depression. However, little is known about the signaling pathways integrating genetic and environmental inputs to impact neurobehavioral outcomes. We report that gut G-protein-coupled receptor, Gpr35, engages a microbe-to-brain metabolic pathway to modulate neuronal plasticity and depressive behavior in mice. Psychological stress decreases intestinal epithelial Gpr35, genetic deletion of which induces depressive-like behavior in a microbiome-dependent manner. Gpr35-/- mice and individuals with depression have increased Parabacteroides distasonis, and its colonization to wild-type mice induces depression. Gpr35-/- and Parabacteroides distasonis-colonized mice show reduced indole-3-carboxaldehyde (IAld) and increased indole-3-lactate (ILA), which are produced from opposing branches along the bacterial catabolic pathway of tryptophan. IAld and ILA counteractively modulate neuroplasticity in the nucleus accumbens, a brain region linked to depression. IAld supplementation produces anti-depressant effects in mice with stress or gut epithelial Gpr35 deficiency. Together, these findings elucidate a gut microbe-brain signaling mechanism that underlies susceptibility to depression.
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Gut microbiota depletion from early adolescence alters adult immunological and neurobehavioral responses in a mouse model of multiple sclerosis.
Emerging evidence indicates that gut microbiota interacts with immune and nervous systems in the host and plays a critical role in the pathogenesis of multiple sclerosis (MS) and many psychiatric disorders such as depression and anxiety. The aim of this study was to explore the influence of gut bacterial depletion from early adolescence on adult immunological and neurobehavioral responses in mice with experimental-autoimmune-encephalomyelitis (EAE). We used an animal model of gut microbiota depletion induced by antibiotics from weaning to adulthood to assess clinical signs, cognitive function and depression-and anxiety-related symptoms in non-EAE and EAE-induced mice. We measured levels of interferon (IFN)-γ, interleukin (IL)-17A and IL-10 in serum, and BDNF, IL-1β and tumor necrosis factor (TNF)-α) in the hippocampus. Antibiotic-treated mice displayed a significant delay in the onset of clinical symptoms of EAE. However, a higher severity of EAE was found between days 19-22 post-immunization in antibiotics-treated mice, while a reduction in the clinical signs of MS was observed at days 24-25 post-immunization. Antibiotic administration decreased IFN-γ and IL-17A levels and increased IL-10 in serum of EAE-induced mice. Antibiotic treatment significantly decreased hippocampal BDNF and enhanced learning and memory impairments in EAE-induced mice. However, no significant changes were found in non-EAE mice. Non-EAE and EAE mice treated with antibiotics exhibited increased anxiety-related behaviors, whereas depression-related symptoms and increased hippocampal TNF-α and IL-1β were only observed in EAE-induced mice treated with antibiotics. This study supports the view that depletion of gut microbiota by antibiotics from weaning profoundly impacts adult immunological and neurobehavioral responses.
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Gut microbiota mediates prenatal METH exposure-induced anxiety- and depression-like behaviors by modulating the Wnt signaling pathway.
Prenatal methamphetamine (METH) exposure poses a significant threat to offspring health, including anxiety and depression-like behaviors. This study investigated the neurotoxicity of prenatal METH exposure in offspring and explored the underlying mechanisms involving the gut microbiota. Our results revealed that prenatal METH exposure induced anxiety- and depression-like behaviors in offspring, accompanied by increased hippocampal inflammation and decreased hippocampal neurogenesis. Importantly, offspring exposed to prenatal METH exhibited gut microbiota dysbiosis, characterized by a reduced abundance of beneficial bacteria and an increased abundance of pro-inflammatory bacteria. To assess the involvement of the gut microbiota, we conducted cross-fostering and inulin supplementation experiments. Cross-fostering with control dams partially reversed METH-induced behavioral deficits, suggesting a role for maternal microbiota transmission. Inulin supplementation, both during pregnancy and in offspring, effectively remodeled the gut microbiota composition and alleviated anxiety and depression-like behaviors. This effect was associated with reduced hippocampal inflammation and increased hippocampal neurogenesis, potentially mediated by activation of the canonical Wnt signaling pathway. This study provides evidence for the critical role of the gut microbiota in mediating the neurodevelopmental consequences of prenatal METH exposure, and highlights the potential of inulin supplementation as a promising therapeutic strategy.
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The Effects of Stress and Diet on the "Brain-Gut" and "Gut-Brain" Pathways in Animal Models of Stress and Depression.
Compelling evidence is building for the involvement of the complex, bidirectional communication axis between the gastrointestinal tract and the brain in neuropsychiatric disorders such as depression. With depression projected to be the number one health concern by 2030 and its pathophysiology yet to be fully elucidated, a comprehensive understanding of the interactions between environmental factors, such as stress and diet, with the neurobiology of depression is needed. In this review, the latest research on the effects of stress on the bidirectional connections between the brain and the gut across the most widely used animal models of stress and depression is summarised, followed by comparisons of the diversity and composition of the gut microbiota across animal models of stress and depression with possible implications for the gut-brain axis and the impact of dietary changes on these. The composition of the gut microbiota was consistently altered across the animal models investigated, although differences between each of the studies and models existed. Chronic stressors appeared to have negative effects on both brain and gut health, while supplementation with prebiotics and/or probiotics show promise in alleviating depression pathophysiology.
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Bacterial Metabolites of Human Gut Microbiota Correlating with Depression.
Depression is a global threat to mental health that affects around 264 million people worldwide. Despite the considerable evolution in our understanding of the pathophysiology of depression, no reliable biomarkers that have contributed to objective diagnoses and clinical therapy currently exist. The discovery of the microbiota-gut-brain axis induced scientists to study the role of gut microbiota (GM) in the pathogenesis of depression. Over the last decade, many of studies were conducted in this field. The productions of metabolites and compounds with neuroactive and immunomodulatory properties among mechanisms such as the mediating effects of the GM on the brain, have been identified. This comprehensive review was focused on low molecular weight compounds implicated in depression as potential products of the GM. The other possible mechanisms of GM involvement in depression were presented, as well as changes in the composition of the microbiota of patients with depression. In conclusion, the therapeutic potential of functional foods and psychobiotics in relieving depression were considered. The described biomarkers associated with GM could potentially enhance the diagnostic criteria for depressive disorders in clinical practice and represent a potential future diagnostic tool based on metagenomic technologies for assessing the development of depressive disorders.
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Study on the efficacy and mechanism of fecal microbiota transplantation for depression based on circadian rhythm.
BACKGROUND: Depression is closely associated with disruptions in circadian rhythms, and emerging evidence highlights critical roles of gut dysbiosis in its pathogenesis. However, the mechanisms by which FMT chronotherapy influences circadian gene in depression-via gut microbiota-remain poorly understood. METHODS: In this study, we established a chronic unpredictable mild stress (CUMS) mouse model and performed fecal microbiota transplantation (FMT) using donor microbiota from healthy mice at two distinct circadian time points-zeitgeber time (ZT) 4 or ZT16 to identify the optimal timing for FMT based on behavioral assessments. Integrating omics dependent mechanisms of antidepressant effects mediated by these key functional bacteria. RESULTS: Health-FMT significantly alleviated depressive-like behaviors, with superior efficacy at ZT4. It restored circadian gene expressions and attenuated neuroinflammation expression in the hippocampus and prefrontal cortex. 16S rRNA sequencing revealed that Health-FMT reduced uncultured_bacterium_g_Alistipes abundance, a genus linked to tryptophan availability. Tryptophan supplementation regulated circadian gene expressions, inflammatory factors, brain-derived neurotrophic factors (BDNF), microglial and astrocytic activation, and exerted antidepressant effects via the ERK signaling pathway. CONCLUSIONS: These findings suggest that Health-FMT exerts antidepressant effects by restoring gut homeostasis, particularly by reducing Alistipes, thereby rebalancing tryptophan metabolic and circadian gene expressions. These findings offer a new possible mechanism and novel insights into the microbiota-gut-brain axis in depression, and underscore the importance of chronotherapy in FMT-based therapeutic strategies.
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Relief from Chronic Unpredictable Mild Stress-Induced Constipation by Fluoxetine and Butyrate and Their Impact on Gut Microecology.
PURPOSE: This study investigated fluoxetine (FLX) effects on chronic unpredictable mild stress (CUMS)-induced depression and constipation, and to explore the potential synergistic benefits of combining FLX with butyrate supplementation. METHODS: A mouse model of CUMS and functional constipation (FC) was established. Behavioral assessments, fecal parameters, colonic transit time, and histological analysis were performed. Serotonin signaling, gastrointestinal hormones, intestinal barrier function, and inflammatory markers were measured. Gut microbiota composition was assessed using 16S rRNA sequencing, and fecal short-chain fatty acid (SCFA) levels were quantified by gas chromatography-mass spectrometry. RESULTS: FLX significantly alleviated depressive-like behaviors (40% reduction in immobility time) and improved gastrointestinal motility (35% increase in fecal pellet output) in CUMS-FC mice. FLX restored serotonin signaling (2.5-fold increase in 5-HT levels), enhanced intestinal barrier integrity (60% upregulation of ZO-1/Occludin), and increased gut microbial diversity (Shannon index increased by 30%). FLX elevated butyrate-producing bacteria and fecal butyrate levels by 45%. Notably, the novel FLX-butyrate combination produced synergistic effects, achieving 65% improvement in gut motility, 70% reduction in pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), and 80% restoration of intestinal barrier function compared to FLX alone. CONCLUSION: FLX alleviates CUMS-induced depression and constipation through restoring serotonin signaling, modulating gut microbiota toward SCFA production, and improving intestinal barrier function. The novel synergistic enhancement achieved by FLX-butyrate combination demonstrates superior therapeutic efficacy, highlighting its potential as an innovative dual-targeting strategy for gut-brain axis disorders.