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Regulation of Neurotransmitters by the Gut Microbiota and Effects on Cognition in Neurological Disorders.
Emerging evidence indicates that gut microbiota is important in the regulation of brain activity and cognitive functions. Microbes mediate communication among the metabolic, peripheral immune, and central nervous systems via the microbiota-gut-brain axis. However, it is not well understood how the gut microbiome and neurons in the brain mutually interact or how these interactions affect normal brain functioning and cognition. We summarize the mechanisms whereby the gut microbiota regulate the production, transportation, and functioning of neurotransmitters. We also discuss how microbiome dysbiosis affects cognitive function, especially in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
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Resistant Starch-Capric Acid Effectively Improves Lipopolysaccharide-Induced Depressive Behavior by Protecting the Intestinal Microbiota Barrier and Inhibiting Inflammatory Responses.
Previous studies have found that gut flora, immunity, and neuroinflammation play key roles in the pathogenesis of depression, and fatty acids are neuroprotective. The present study aimed to reveal the effects of capric acid intake (absorbed in the colon via resistant starch complex) on LPS-induced depression-like behavior and its underlying mechanisms. Male ICR mice were ingested with resistant starch-decanoic acid complex (RS-FA, 13 g/kg) for 50 consecutive days. The depression model was established by injecting LPS (0.5 mg/kg every two days for three injections). The results of behavioral tests showed that the mice pretreated with resistant starch capric acid complex had significantly shorter resting time in the tail suspension test (TST); the number of crossing grids and the number of standing in the open field test (OFT) were significantly increased. In addition, TNF-α levels in the serum of depressed mice were decreased; 5-HT levels in the hippocampus were increased. It had an ameliorative effect on the haphazard arrangement of colonic glandular cells caused by LPS, as well as nuclear condensation and eosinophilic degeneration of hippocampal neurons. 16S rRNA analysis revealed that pretreatment with resistant starch-capric acid complexes reversed depression-associated dysbiosis, restoring gut microbial composition to levels approaching those of the control group. Restores uniformity in the animal gut microbiota, increases beneficial bacterial populations, and demonstrates efficacy in elevating short-chain fatty acid levels. Furthermore, resistant starch-capric acid concurrently modulates the TLR4/NF-κB signaling pathway and the tryptophan metabolic pathway to regulate gut microbiota dysbiosis in depressed mice.
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The Role of Gut-Brain Tryptophan Metabolism and Fatty Acid Peroxidation in the Effect of Sleep Deprivation on Anxiety and Depression in PCOS Mice.
Polycystic ovary syndrome (PCOS) is the most prevalent endocrine disorder in women of childbearing age. Numerous studies have indicated a significantly elevated incidence of depression and anxiety in women affected by PCOS, often attributed to dysbiosis of gut microbiota resulting from poor sleep quality. However, the intricate relationship between sleep disorders, gut microbiota, and depression/anxiety in PCOS remains unclear. In this study, we aimed to elucidate the effects of sleep deprivation on the anxiety and depression of PCOS mice through an investigation of the gut-brain axis in order to understand the potential microbial-host interactions contributing to the occurrence of these psychological disorders. We found that sleep deprivation induced symptoms of depression and anxiety in PCOS mice and exacerbated PCOS-like pathology. Moreover, sleep deprivation altered the gut microbiota composition by suppressing beneficial bacteria such as Lactobacillus and Ruminococcus species. Additionally, sleep deprivation upregulated intestinal tryptophan-kynurenine metabolism, increased intestinal wall permeability, promoted systemic inflammation, and compromised blood-brain barrier integrity. Furthermore, the hippocampal metabolomic analysis indicated that sleep deprivation affected the metabolism of fatty acid and oxylipins, upregulated the tryptophan-kynurenine metabolic pathway, and exhibited a significant correlation with anxiety and depressive behaviors. Overall, this study suggests that sleep deprivation plays a pivotal role in the pathological mechanism of depression and anxiety in PCOS mice by modulating tryptophan and lipid metabolism through the gut-brain axis.
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Metabolomic signatures and microbial community profiling of depressive rat model induced by adrenocorticotrophic hormone.
BACKGROUND: Adrenocorticotrophic hormone (ACTH)-treatment rat model has been utilized as a widely accepted model of treatment-resistant depression. Metabolomic signatures represent the pathophysiological phenotype of diseases. Recent studies in gut microbiota and metabolomics analysis revealed the dramatic role of microbiome in psychoneurological system diseases, but still, the mechanisms underlying gut microbiome-host interaction remain unclear. METHODS: Male Wistar rats were s.c. injection of ACTH fragment 1-24 for 14 days to induce treatment-resistant depression. Depression-related behavioral tests, analysis of serum monoamine neurotransmitters and hypothalamic-pituitary-adrenal (HPA) axis-related hormones were determined for assessment of ACTH-induced depression rat model. A gas chromatography-time-of-flight mass spectrometer based urinary metabolomic signatures integrated 16S rRNA sequence analysis based gut microbial profiling was performed, as well as Spearman's correlation coefficient analysis was used to manifest the covariation between the differential urinary metabolites and gut microbiota of genus level. RESULTS: Chronic injection of ACTH-induced depression-like phenotype (increased immobility time in forced swimming test and tail suspension test) was accompanied by peripheral serotonin down-regulation and HPA axis overactivation (ACTH and corticosterone up-regulation). Urinary metabolomics analysis indicated that pyruvic acid, L-threonine, mannitol, D-gluconic acid, 4-hydroxybenzoic acid, D-arabitol, myo-inositol and ascorbic acid levels were reduced in ACTH-treated rats' urine, while hippurate level was elevated. In addition, microbial community profiling revealed bacterial enrichment (e.g. Ruminococcus, Klebsiella) and reduction (e.g. Akkermansia, Lactobacillus) in the ACTH-induced depression rat model. Correlation analysis showed that Akkermansia and Lactobacillus were closely relevant to metabolites myo-inositol and hippurate, which were included in host inositol phosphate metabolism, and phenylalanine, tyrosine and tryptophan biosynthesis. CONCLUSIONS: Depression rat model induced by ACTH is associated with disturbance of pyruvate metabolism, ascorbate and aldarate metabolism, inositol phosphate metabolism, glycine, serine and threonine metabolism, and glycolysis or gluconeogenesis, as well as changes in microbial community structure. Gut microbiota may participate in the mediation of systemic metabolomic changes in ACTH-induced depression model. Therefore, integrated metabolomic signatures and gut microbial community profiling would provide a basis for further studies on the pathogenesis of depression.
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Gut Feeling: Researchers Are Discovering a Link Between Depression and Gut Bacteria.
The human gut is home to an abundant and diverse community of microbes–each of us carries roughly 100 trillion, representing more than 1,000 different species. The composition of one?s gut microbiota is individually specific, dynamic, and influenced by genetics, diet, age, metabolism, medication use, stress, and geography. These bacteria perform a range of necessary and beneficial functions, including breaking down our food and supporting our immune systems.
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Profiles of gut microbiota and metabolites for high risk of transgenerational depression-like behavior by paternal methamphetamine exposure.
Parental substance abuse increases the risk of neurological and psychiatric disorders in offsprings. However, its underlying mechanism remains elusive. Our previous study demonstrated that long-term exposure to methamphetamine (Meth), a psychostimulant drug with high addiction potential, remarkably alters the gut microbiome and metabolites in male mice, which contribute to Meth-induced anxiety-like behaviors. The current study aimed to investigate whether gut microbiota and metabolism serve as potential peripheral targets for transgenerational mental problems by paternal Meth exposure. We found that paternal Meth exposure induced depression-like behaviors both in the first (F1) and the second (F2) generations of male mice. Further, the depletion of gut bacteria through antibiotic treatments normalized the depression-like behaviors to normal levels in both F1 and F2 male mice. Then, alterations in gut bacterial composition were observed in both F1 and F2 male mice. Specifically, Eubacterium_ruminantium_group, Enterorhabdus, Alloprevotella, and Parabacteroides were the commonly affected bacterial taxa in F1 and F2 male mice. In addition, the results of alterations in gut metabolism showed that LPC 14:1-SN1 emerged as the consistently altered metabolite in the colons of F1 and F2 male mice. Taken together, our findings provide the first evidence that paternal Meth exposure enhances depression-like behaviors in F1 and F2 male mice, potentially mediated by the gut microbiome and metabolism.
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Dietary magnesium deficiency alters gut microbiota and leads to depressive-like behaviour.
OBJECTIVE: Gut microbiota (GM) has previously been associated with alterations in rodent behaviour, and since the GM is affected by the diet, the composition of the diet may be an important factor contributing to behavioural changes. Interestingly, a magnesium restricted diet has been shown to induce anxiety and depressive-like behaviour in humans and rodents, and it could be suggested that magnesium deficiency may mediate the effects through an altered GM. METHODS: The present study therefore fed C57BL/6 mice with a standard diet or a magnesium deficient diet (MgD) for 6 weeks, followed by behavioural testing in the forced swim test (FST) to evaluate depressive-like behaviour. An intraperitoneal glucose tolerance test (GTT) was performed 2 day after the FST to assess metabolic alterations. Neuroinflammatory markers were analysed from hippocampus. GM composition was analysed and correlated to the behaviour and hippocampal markers. RESULTS: It was found that mice exposed to MgD for 6 weeks were more immobile than control mice in the FST, suggesting an increased depressive-like behaviour. No significant difference was detected in the GTT. GM composition correlated positively with the behaviour of undisturbed C57BL/6 mice, feeding MgD diet altered the microbial composition. The altered GM correlated positively to the hippocampal interleukin-6. CONCLUSION: In conclusion, we hypothesise that imbalances of the microbiota-gut-brain axis induced by consuming a MgD diet, contributes to the development of depressive-like behaviour.
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The Perinatal Microbiota-Gut-Brain Axis: Implications for Postpartum Depression.
BACKGROUND: Pregnancy and childbirth are accompanied by widespread maternal physiological adaptations and hormonal shifts that have been suggested to result in a period of vulnerability for the development of mood disorders such as postpartum depression (PPD). There is also evidence of peripartum changes in the composition of the gut microbiota, but the potential contribution of intestinal microbes to the adaptations, or subsequent vulnerabilities, during this period are unknown. SUMMARY: Here, we outline key pathways involved in peripartum adaptations including GABAergic signaling, oxytocin, and immunomodulation that are also associated with susceptibility to mood disorders and present evidence that these pathways are modulated by gut microbes. We also discuss the therapeutic potential of the microbiota-gut-brain axis in PPD and identify future directions for research to help realize this potential. KEY MESSAGES: Peripartum adaptations are associated with shifts in gut microbial composition. Disruption of GABAergic, oxytocin, and immunomodulatory pathways may contribute to vulnerability of mood disorders including PPD. These key adaptive pathways are modulated by intestinal microbes suggesting a role for the gut microbiota in determining susceptibility to PPD. More research is needed to confirm relationship between gut microbes and PPD and to gain the mechanistic understanding required to realize the therapeutic potential of microbiota-gut-brain axis in this mood disorder.
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Akkermansia muciniphila reverses neuronal atrophy in Negr1 knockout mice with depression-like phenotypes.
Genetic predispositions can shape the gut microbiome, which in turn modulates host gene expression and impacts host physiology. The complex interplay between host genetics and the gut microbiome likely contributes to the development of neuropsychiatric disorders, yet the mechanisms behind these interactions remain largely unexplored. In this study, we investigated the gut microbiota in Negr1 knockout (KO) mice, which exhibit anxiety- and depression-like behaviors, as NEGR1 (neuronal growth regulator 1) is a cell adhesion molecule linked to neuronal development and neuropsychiatric disorders. Our findings show significant early-life alterations in the gut microbiota composition of Negr1 KO mice, most notably a marked reduction in Akkermansia spp. along with reduced dendritic arborization and spine density in the nucleus accumbens (NAc) and the dentate gyrus (DG) of the hippocampus. Remarkably, daily administration of an Akkermansia strain isolated from wild-type mice reversed the neuronal structural abnormalities and ameliorated anxiety- and depression-like behaviors in Negr1 KO mice. Transcriptomic profiling revealed upregulation of mitochondrial genome-encoded genes in the NAc and hippocampus of Negr1 KO mice, along with a predisposition toward a pro-inflammatory state in the colon of Negr1 KO mice. The Akkermansia supplementation downregulated these mitochondrial genes in the NAc and hippocampus and upregulated genes involved in T cell activation and immune homeostasis in the colon. These findings demonstrate a novel gene-microbiome interaction in the pathophysiology of Negr1 KO mice, positioning Akkermansia spp. as a key mediator that improves neuronal atrophy and modulates anxiety- and depression-like behaviors. Our study provides compelling evidence for bidirectional interactions between host genetics and the gut microbiome in modulating neuropsychiatric phenotypes, offering new insights for addressing genetically influenced mental disorders.
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Microbes and mood: innovative biomarker approaches in depression.
Although the field of psychiatry has made gains in biomarker discovery, our ability to change long-term outcomes remains inadequate. Matching individuals to the best treatment for them is a persistent clinical challenge. Moreover, the development of novel treatments has been hampered in part due to a limited understanding of the biological mechanisms underlying individual differences that contribute to clinical heterogeneity. The gut microbiome has become an area of intensive research in conditions ranging from metabolic disorders to cancer. Innovation in these spaces has led to translational breakthroughs, offering novel microbiome-informed approaches that may improve patient outcomes. In this review we examine how translational microbiome research is poised to advance biomarker discovery in mental health, with a focus on depression.