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Cubebin alleviates chronic stress-induced depression-like behavior in mice by regulating the gut microbiome.
The gut-brain axis is dysregulated as a consequence of alterations in the gut microbiota. These alterations increase toxic microbial metabolites, endotoxemia, and the release of immune mediators and contribute to the development of depression. Cubebin is a dibenzyl butyrolactone lignan, and its stem is also known as Agaru in Tibetan areas, it is commonly used as a sedative and tranquilizing medicine. This study aimed to investigate the effects of cubebin on chronic stress-induced depression-like behavior in mice. Cubebin was observed to mitigate depressive-like behavior in chronic unpredictable mild stress (CUMS) mice, influence the restoration of their cerebral cortex and hippocampal tissue morphology, and enhance the abundance of relevant intestinal flora in depression model mice, particularly by decreasing the abundance of Clostridium, Dorea, and Ruminococcus. The final protein function expression was normalized by regulating depression-related metabolic pathways. Concomitantly, the concentrations of neurotransmitters serotonin (5-HT), norepinephrine (NE), and dopamine (DA) in the brains of mice in the model group were enhanced, and their depressive symptoms were mitigated. Our study findings suggest that cubebin may ameliorate CUMS-induced depression in mice by modulating the microbe-gut-brain axis, elucidating the key effect of gut metabolites on depressive symptoms.
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Precision medicine in perinatal depression in light of the human microbiome.
Perinatal depression is the most common complication of pregnancy and affects the mother, fetus, and infant. Recent preclinical studies and a limited number of clinical studies have suggested an influence of the gut microbiome on the onset and course of mental health disorders. In this review, we examine the current state of knowledge regarding genetics, epigenetics, heritability, and neuro-immuno-endocrine systems biology in perinatal mood disorders, with a particular focus on the interaction between these factors and the gut microbiome, which is mediated via the gut-brain axis. We also provide an overview of experimental and analytical methods that are currently available to researchers interested in elucidating the influence of the gut microbiome on mental health disorders during pregnancy and postpartum.
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Gut-Brain Axis and Behavior.
In the last 5 years, interest in the interactions among the gut microbiome, brain, and behavior has exploded. Preclinical evidence supports a role of the gut microbiome in behavioral responses associated with pain, emotion, social interactions, and food intake. Limited, but growing, clinical evidence comes primarily from associations of gut microbial composition and function to behavioral and clinical features and brain structure and function. Converging evidence suggests that the brain and the gut microbiota are in bidirectional communication. Observed dysbiotic states in depression, chronic stress, and autism may reflect altered brain signaling to the gut, while altered gut microbial signaling to the brain may play a role in reinforcing brain alterations. On the other hand, primary dysbiotic states due to Western diets may signal to the brain, altering ingestive behavior. While studies performed in patients with depression and rodent models generated by fecal microbial transfer from such patients suggest causation, evidence for an influence of acute gut microbial alterations on human behavioral and clinical parameters is lacking. Only recently has an open-label microbial transfer therapy in children with autism tentatively validated the gut microbiota as a therapeutic target. The translational potential of preclinical findings remains unclear without further clinical investigation.
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Reduced gut microbiome alpha diversity associates with depressive symptom severity and somatic symptom burden in major depression.
OBJECTIVE: Alteration in gut microbiome have been increasingly linked to many psychiatric disorders inclusive depression. However, findings regarding microbiome diversity in depression remain inconsistent. Differences in depression subtypes, particularly the somatic versus affective symptoms profiles may partly explain this heterogeneity in previous results. METHODS: This cross-sectional study included 31 Participants diagnosed with major depressive disorder. The participants divided into two groups by severity of depression (BDI-II >34 vs. <34) and severity of somatic symptoms of depression (somatic dimension vs. cognitive-affective dimension of BDI-II). Fecal samples were collected, and 16S rRNA gene sequencing of the V3/V4 region was performed on an Illumina platform to profile the gut microbiome. Amplicon Sequence Variants (ASVs) were used to analyze microbial alpha diversity, including ACE, Chao1 and Shannon. RESULTS: Participants with higher depressive severity showed significantly reduced gut microbiome alpha diversity compared to lower depressive state (ACE; p = 0.019, Chao1; p = 0.019, and Shannon; p = 0.053). Across the total sample, BDI-II total score correlated negatively with alpha diversity significantly for ACE (r = -0.435, p = 0.015), Chao1 (r = -0.435, p = 0.015) and Shannon (r = -0.376, p = 0.037). While the somatic dimension of the BDI-II showed significant negative correlation with all tested alpha diversity indices, no significant correlations were detected between gut microbiome alpha diversity and the cognitive-affective dimension. Shannon diversity further correlated negatively with HDRS-17 scores (p = 0.033). CONCLUSION: In conclusion, the results show that a lower diversity of gut microbiota alpha is linked to more severe depressive symptoms, specifically the somatic aspect of depression. These results emphasize the importance of considering somatic symptom profiles in microbiome research and point to the gut-brain axis as a potential target for future therapeutic interventions.
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Gut Microbiome Composition and Its Association with Sleep in Major Psychiatric Disorders.
INTRODUCTION: Sleep disturbances are highly prevalent across most major psychiatric disorders. Alterations in the hypothalamic-pituitary-adrenal axis, neuroimmune mechanisms, and circadian rhythm disturbances partially explain this connection. The gut microbiome is also suspected to play a role in sleep regulation, and recent studies suggest that certain probiotics, prebiotics, synbiotics, and fecal microbiome transplantation can improve sleep quality. METHODS: We aimed to assess the relationship between gut-microbiota composition, psychiatric disorders, and sleep quality in this cross-sectional, cross-disorder study. We recruited 103 participants, 63 patients with psychiatric disorders (major depressive disorder [n = 31], bipolar disorder [n = 13], psychotic disorder [n = 19]) along with 40 healthy controls. Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). The fecal microbiome was analyzed using 16S rRNA sequencing, and groups were compared based on alpha and beta diversity metrics, as well as differentially abundant species and genera. RESULTS: A transdiagnostic decrease in alpha diversity and differences in beta diversity indices were observed in psychiatric patients, compared to controls. Correlation analysis of diversity metrics and PSQI score showed no significance in the patient and control groups. However, three species, Ellagibacter isourolithinifaciens, Senegalimassilia faecalis, and uncultured Blautia sp., and two genera, Senegalimassilia and uncultured Muribaculaceae genus, were differentially abundant in psychiatric patients with good sleep quality (PSQI >8), compared to poor-sleep quality patients (PSQI ≤8). CONCLUSION: In conclusion, this study raises important questions about the interconnection of the gut microbiome and sleep disturbances.
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A Scoping Review on the Role of the Microbiome as a Factor in the Bidirectional Association Between Obesity and Depression.
PURPOSE OF REVIEW: Obesity is a chronic illness highly comorbid with mental health conditions, particularly depression. Among the factors involved in this association, inflammation is a consistently identified link. This review explores the emerging role of the gut microbiota as a modulator of inflammation and its potential involvement in the pathophysiological processes linking obesity and depression. RECENT FINDINGS: Chronic low-grade inflammation is observed in both obesity and depressive disorders. Alterations in gut microbiota are increasingly implicated in inflammatory mechanisms, including increased intestinal permeability, immune activation, and short-chain fatty acid (SCFA) production, influencing leukocyte function and cytokine production. Additionally, both obesity and depression are associated with altered microbial composition. The gut microbiome contributes to chronic inflammation relevant to the pathophysiology of both obesity and depression. Accumulating evidence highlights the need for further research into how gut microbiota influences inflammatory mechanisms observed in both obesity and depression.
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Gut microbiota reshapes host energy metabolism to modulate depressive behaviors.
Disturbances in energy metabolism are a key pathophysiological feature of major depressive disorder (MDD). The gut microbiota, as a critical regulator of host metabolism, may influence systemic energy homeostasis and contribute to depression. To investigate this, we performed a multi-omics analysis integrating targeted metabolomics and shotgun metagenomics on samples from 100 MDD patients and 68 healthy controls. MDD patients exhibited significant disruptions in central energy pathways (glycolysis, TCA cycle, and ornithine cycle), which correlated with symptom severity and cognitive impairment. We identified 36 bacterial species whose abundances were linked to mitochondrial fatty acid synthesis, ketogenesis, and amino acid metabolism, and were associated with altered levels of core metabolites like lactate and L-glutamic acid. Mediation analysis established a "gut microbiota-energy metabolites-depressive phenotype" axis, where metabolites mediated the effects of specific bacteria (e.g., Dorea_formicigenerans) on symptoms. To validate causality, we used a chronic social defeat stress mouse model with simultaneous autologous fecal microbiota transplantation (FMT). FMT effectively reshaped the gut microbiota, ameliorated depression-like behaviors, and reversed the stress-induced shift toward anaerobic glycolysis in serum and the central nervous system. Critically, FMT restored mitochondrial morphology and structural integrity in the prefrontal cortex and hippocampus, renormalizing the relationship between metabolism and behavior. Our findings elucidate the gut microbiota's role in MDD pathogenesis via host energy metabolism regulation and posit early autologous FMT as a novel strategy to correct central energy imbalances.
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Moody microbiome: Challenges and chances.
Growing evidence link gut microbiome to the development and maturation of the central nervous system, which are regulated by microbiota potentially through stress response, neurotransmitter, neuroimmune, and endocrine pathways. The dysfunction of such microbiota-gut-brain axis is implicated in neuropsychiatric disorders, depression, and other stress-related conditions. Using affective disorders as our primary outcomes, we inspect the current evidence of microbiota studies mainly in human clinical samples. Additionally, to restore microbiome equilibrium in bacteria diversity and abundance might represent a novel strategy to prevent or treat mood symptoms. We reviewed findings from clinical trials regarding efficacy of probiotics supplement with or without antidepressant treatment, and adjuvant antimicrobiotics treatment. In microbiota studies, the considerations of host-microbiota interaction and bacteria-bacteria interaction are discussed. In conclusion, the roles of microbiota in depression and mania state are not fully elucidated. One of the challenges is to find reliable targets for functional analyses and experiments. Notwithstanding some inconsistencies and methodological limitations across studies, results from recent clinical trials support for the beneficial effects of probiotics on alleviating depressive symptoms and increasing well-beings. Moreover, modifying the composition of gut microbiota via antibiotics can be a viable adjuvant treatment option for individuals with depressive symptoms.
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Mitigation and mechanism of low dose linoleic acid on depression caused by disorder of gut microbiome.
OBJECTIVES: Depression is a widely prevalent mental disorder, and nutritional interventions play an increasingly important role in its treatment. In this paper, effects of linoleic acid (LA) on depressive behavior in mice induced by gut microbiome disorders were investigated. METHODS: Fifty C57BL/6J male mice were randomly separated into five groups, control group (CK), ceftriaxone sodium group (CRO), low-dose linoleic acid group (LLA, 1 g/kg), medium-dose linoleic acid group (MLA, 2 g/kg), and high-dose linoleic acid group (HLA, 5 g/kg). In the LLA, MLA, and HLA groups, mice were treated with ceftriaxone sodium (CRO) to induce depressive behaviors, followed by LA administration. Behavioral tests were used to evaluate depressive behavior. High-throughput sequencing and Hematoxylin-eosin (H&E) staining in gut microenvironment were carried out. ELISA kits were used to measure brain inflammatory factors, and 5-hydroxy-tryptamine (5-HT). Gas chromatography and western blot were used to determine fatty acids compositions and the enzymes expression involved in lipid metabolism in brain respectively. RESULTS: The results showed that 10 weeks CRO treatment contribute to depressive behavior, gut microbiome disturbance, and serotonin system disturbance. LLA and MLA improved the depressive-like behavior, and significantly increased the levels of 5-HT1A, 5-HTT and 5-HT in the hippocampus. LLA was found to improve the diversity of gut microbiome and alleviate colon tissue damage. Meantime, LLA increased the content of linoleic acid, improved the expression of FADS2 and COX-2, increased IL-10 levels, and decreased IL-6 levels in the brain. DISCUSSION: LA alleviated depressive behavior in mice by improving the gut microenvironment, regulate fatty acid metabolism, and modulate inflammation.
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Role of the Intestinal Microbiome, Intestinal Barrier and Psychobiotics in Depression.
The intestinal microbiota plays an important role in the pathophysiology of depression. As determined, the microbiota influences the shaping and modulation of the functioning of the gut-brain axis. The intestinal microbiota has a significant impact on processes related to neurotransmitter synthesis, the myelination of neurons in the prefrontal cortex, and is also involved in the development of the amygdala and hippocampus. Intestinal bacteria are also a source of vitamins, the deficiency of which is believed to be related to the response to antidepressant therapy and may lead to exacerbation of depressive symptoms. Additionally, it is known that, in periods of excessive activation of stress reactions, the immune system also plays an important role, negatively affecting the tightness of the intestinal barrier and intestinal microflora. In this review, we have summarized the role of the gut microbiota, its metabolites, and diet in susceptibility to depression. We also describe abnormalities in the functioning of the intestinal barrier caused by increased activity of the immune system in response to stressors. Moreover, the presented study discusses the role of psychobiotics in the prevention and treatment of depression through their influence on the intestinal barrier, immune processes, and functioning of the nervous system.