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SAD rats: Effects of short photoperiod and carbohydrate consumption on sleep, liver steatosis, and the gut microbiome in diurnal grass rats.
Seasonal affective disorder (SAD) is a recurrent depression triggered by exposure to short photoperiods, with a subset of patients reporting hypersomnia, increased appetite, and carbohydrate craving. Dysfunction of the microbiota - gut - brain axis is frequently associated with depressive disorders, but its role in SAD is unknown. Nile grass rats (Arvicanthis niloticus) are potentially useful for exploring the pathophysiology of SAD, as they are diurnal and have been found to exhibit anhedonia and affective-like behavior in response to short photoperiods. Further, given grass rats have been found to spontaneously develop metabolic syndrome, they may be particularly susceptible to environmental triggers of metabolic dysbiosis. We conducted a 2 × 2 factorial design experiment to test the effects of short photoperiod (4 h:20 h Light:Dark (LD) vs. neutral 12:12 LD), access to a high concentration (8%) sucrose solution, and the interaction between the two, on activity, sleep, liver steatosis, and the gut microbiome of grass rats. We found that animals on short photoperiods maintained robust diel rhythms and similar subjective day lengths as controls in neutral photoperiods but showed disrupted activity and sleep patterns (i.e. a return to sleep after an initial bout of activity that occurs ~ 13 h before lights off). We found no evidence that photoperiod influenced sucrose consumption. By the end of the experiment, some grass rats were overweight and exhibited signs of non-alcoholic fatty liver disease (NAFLD) with micro- and macro-steatosis. However, neither photoperiod nor access to sucrose solution significantly affected the degree of liver steatosis. The gut microbiome of grass rats varied substantially among individuals, but most variation was attributable to parental effects and the microbiome was unaffected by photoperiod or access to sucrose. Our study indicates short photoperiod leads to disrupted activity and sleep in grass rats but does not impact sucrose consumption or exacerbate metabolic dysbiosis and NAFLD.
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Chronic airway inflammation is associated with sex-dependent changes in behaviour, neuroinflammation and the gut microbiome.
Asthma is a chronic inflammatory lung disease linked to a higher prevalence of comorbid mood disorders, such as anxiety and depression, though the underlying pathophysiology and the influence of biological sex remain poorly understood. To investigate this complex relationship, we employed a chronic house dust mite (HDM) exposure model in male and female C57BL/6 mice, examining the sex-dependent effects of allergic airway inflammation across systemic, neuroimmune, behavioural, and gut microbiome axes. Chronic HDM exposure successfully induced hallmark features of allergic airway disease in both sexes. While females exhibited significantly higher levels of most measured airway and systemic inflammatory cytokines compared to males, the neuroinflammatory and behavioural changes were more pronounced in males. HDM-exposed males showed increased hippocampal microglial activation, enhanced mast cell presence, and widespread hypothalamic transcriptional alterations. Females, however, exhibited increased astrocytic activation and enrichment of the estrogen response pathway, suggesting a differential, potentially protective, glial responses. Behaviourally, males displayed reduced grooming and greater despair-like behaviour, consistent with depressive-like phenotypes, whereas females showed reduced grooming only. Parallel analyses revealed that males experienced more extensive gut microbial disruption, particularly in the small intestine, including reductions in taxa previously associated with depressive behaviours (Romboutsia, Turicibacter) and broader shifts in microbial metabolic pathways. The observation that males, despite lower systemic inflammation, exhibit greater neuroinflammatory signatures, more extensive hypothalamic changes, and distinct behavioural deficits underscores the necessity of a sex-informed approach to understanding and mitigating the neuropsychiatric sequelae of chronic allergic asthma.
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Anti-depressive-like and cognitive impairment alleviation effects of Gastrodia elata Blume water extract is related to gut microbiome remodeling in ApoE-/- mice exposed to unpredictable chronic mild stress.
ETHNOPHARMACOLOGY RELEVANCE: Gastrodia elata Blume (GE) is a traditional Chinese dietary therapy used to treat neurological disorders. Gastrodia elata Blume water extract (WGE) has been shown to ameliorate inflammation and improve social frustration in mice in a chronic social defeat model. However, studies on the anti-depressive-like effects and cognitive impairment alleviation related to the impact of WGE on the gut microbiome of ApoE-/- mice remain elusive. AIM OF THE STUDY: The present study aimed to investigate the anti-depressive-like effect and cognitive impairment alleviation and mechanisms of WGE in ApoE-/- mice subjected to unpredictable chronic mild stress (UCMS), as well as its impact on the gut microbiome of the mice. MATERIALS AND METHODS: Sixty ApoE-/- mice (6 months old) were randomly grouped into six groups: control, UCMS, WGE groups [5, 10, 20 mL WGE/kg body weight (bw) + UCMS], and a positive group (fluoxetine 20 mg/kg bw + UCMS). After four weeks of the UCMS paradigm, the sucrose preference, novel object recognition, and open field tests were conducted. The neurotransmitters serotonin (5-HT), dopamine (DA) and their metabolites were measured in the prefrontal cortex. Serum was collected to measure corticosterone and amyloid-42 (Aβ-42) levels. Feces were collected, and the gut microbiome was analyzed. RESULTS: WGE restored sucrose preference, exploratory behavior, recognition ability, and decreased the levels of serum corticosterone and Aβ-42 in ApoE-/- mice to alleviate depressive-like behavior and cognitive impairment. Furthermore, WGE regulated the monoamine neurotransmitter via reduced the 5-HT and DA turnover rates in the prefrontal cortex. Moreover, WGE elevated the levels of potentially beneficial bacteria such as Bifidobacterium, Akkermansia, Alloprevotella, Defluviitaleaceae_UCG-011, and Bifidobacterium pseudolongum as well as balanced fecal short-chain fatty acids (SCFAs). CONCLUSION: WGE demonstrates anti-depressive-like effects, cognitive impairment alleviation, and gut microbiome and metabolite regulation in ApoE-/- mice. Our results support the possibility of developing a functional and complementary medicine to prevent or alleviate depression and cognitive decline using WGE in CVDs patients.
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Gut Microbiome and Psychoneurological Symptoms Among Patients With Colorectal Cancer and Their Caregivers: A Pilot Study.
Purpose: Survivorship in colorectal cancer (CRC) is often accompanied by co-occurring psychoneurological symptoms (PNS, e.g., fatigue, depression, pain), which negatively affect quality of life. Caregivers of individuals with CRC also experience PNS due to caregiving burdens, amplifying distress across the dyad. PNS may be influenced by the activity of the gut microbes. The purpose of this pilot study was to examine gut microbiome diversity and composition, and their association with PNS in CRC patients and their caregivers. Methods: Baseline data from a technology-based dyadic intervention were included in this analysis. Eleven patients and eight caregivers provided stool samples and completed PROMIS measures of PNS at baseline. Gut microbiome profiles were assessed using 16S rRNA gene sequencing. Alpha and beta diversity metrics and differential abundance analyses were used to characterize the gut microbiome and examine its associations with PNS. Results: Patients exhibited significantly lower microbial alpha diversity than caregivers in the full sample (p = 0.033). Dyadic comparisons identified 92 differentially abundant taxa, with patients showing depletion of short-chain fatty acid-producing taxa and enrichment of opportunistic taxa. Microbiome-symptom models revealed significant interactions by group (patient vs. caregiver) and taxa-level effects, with patients showing stronger positive associations between microbial alterations and higher PNS severity. Conclusions: CRC patients actively on chemotherapy demonstrated reduced diversity and depletion of beneficial taxa that may contribute to heightened PNS. Caregivers, despite healthier profiles, reported substantial symptom burden that were linked to gut microbiome features, highlighting dyadic interdependence and the potential for microbiome-targeted, dyadic interventions in survivorship care.
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Stress-induced VIPergic activation mediates microbiota/Th17cell-dependent depressive-like behaviors.
Chronic stress often has deleterious effects leading to the development of psychiatric diseases. The gut-brain axis represents a novel avenue for stress research. The negative effects of stress on the gut physiology have been well-described, whereas the pathways whereby stress controls microbial composition to modulate behaviors remains mainly unknown. We discovered that vasoactive intestinal peptide (VIP) activation promoted stress-induced microbial changes leading to increased infiltration of T helper (Th) 17 cells and microglial activation in the hippocampus and depressive-like behaviors, uncovering a close crosstalk between intestinal VIPergic release and the gut microbiota during stress and providing a new interaction between the nervous system and the gut microbiome after stress. Neutralization of the signature cytokine of Th17 cells, interleukin (IL)-17A, was sufficient to block depressive-like behaviors, reduce neuronal VIPergic activation and microglia activation induced by VIPergic activation after stress, opening new potential therapeutic targets for depression.
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Understanding the Connection Between the Gut-Brain Axis and Major Depression: A Theoretical Perspective.
The theory of neuroinflammation, which is proposed to explain the etiopathogenesis of neuropsychiatric disorders, has a very old history. This theory claims that low-intensity bodily inflammation negatively affects the neuronal system, synaptic neurotransmission is impaired, dysfunction occurs in neurons and glial cells, and because of all these, neuropsychiatric disorders occur. Intestinal microbiota disorder (dysbiosis) is suggested as the source of systemic inflammation. Depression is the disease in which the theory of neuroinflammation is most researched in an experimental environment. The causality between depression and intestinal dysbiosis has not been determined definitively in the studies. Our main goals in this article are to explain how dysbiosis occurs and the effect of civilization on the microbiota, as well as to make a future projection shaped by postmodern living conditions. In order to clarify the concepts, we will draw an analogy between neuroinflammation and a black hole. We will discuss whether we can learn some lessons from this analogy. Finally, we will end our article by making some speculations about the future that awaits humanity. Before we do all this, we will try to briefly explain what neuroinflammation is, its importance and the gut-brain axis.
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Gut Microbiome Associations With Depressive Symptoms in Women With Gynecologic Cancer: A Longitudinal Study.
About one-quarter of women diagnosed with gynecologic cancer experience depressive symptoms. While the precise mechanism remains unclear, little is known about the association between gut microbiota and depressive symptoms in gynecologic cancer. Thus, this study aimed to evaluate the associations between gut microbiota and depressive symptoms in women with gynecologic cancer over cancer treatment. Thirty-seven women with cervical or endometrial cancer were followed at pre-treatment (T0), 6-8 weeks (T1), and 6 months post-radiation (T2). Depressive symptoms were assessed using the Patient Health Questionnaire-9 (PHQ-9). Rectal swabs were collected at each visit and sequenced for the V4 region of the 16S rRNA gene. MaAsLin2 models evaluated cross-sectional associations between gut microbial taxa and depressive symptoms at each time point, whereas GEE models assessed longitudinal associations over the course of cancer treatment. The patients had an average age of 60 years, and 43% were Black. At baseline (T0), 24% of patients exhibited depressive symptoms, which decreased to 21% at T1 and further to 13% at T2. GEE models showed that lower α-diversity (Shannon index, p = 0.05), dissimilar β-diversity (Bray-Curtis distance, p = 0.02), and reduced abundance of the genus Ruminococcus (p = 0.02) were predictive factors associated with depressive symptoms throughout cancer treatment. Higher depressive symptoms were longitudinally associated with lower gut microbial Shannon diversity, dissimilar microbial community composition, and lower abundance of the genus Ruminococcus. Larger longitudinal studies using shotgun metagenomic sequencing are needed to validate these findings and further elucidate the microbial mechanisms underlying depressive symptoms in women with gynecologic cancers.
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Psychobiome Feeding Mind: Polyphenolics in Depression and Anxiety.
Recently gut bacterial populations seem to be involved in many functions and in the pathogenesis of several medical conditions. Traditionally the intestinal microbiome has been recognized to play an important role in metabolizing food compounds in simpler chemical structures for the absorption of different nutrients, and in maintenance control of gastrointestinal pathogens species. Bacterial populations are implicated in a complicated network of interactions within the immune system, epithelial cells local endocrine system, that affects the peripheral and the central nervous system, via blood circulation. Microbiome influencing the mind via immune, endocrine and metabolic signalling, is able to exert some clinical effects in different mental diseases. It releases endocrine substances through several pathways involved in the modulation of neuroinflammation and production of several neurotrasmitter precursors. It has recently been named psychobiome. It is known that phenolic compounds are able to influence microbiome proliferation and to exert several roles, especially regarding neuroinflammation in depressive and anxious behaviour. The clinical effects are reported in the literature. The aim of this study is to highlight the interaction between polyphenols and microbiota- gut-brain axis.
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Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative, and nitrosative stress; tryptophan catabolite; and gut-brain pathways.
The nature of depression has recently been reconceptualized, being conceived as the clinical expression of activated immune-inflammatory, oxidative, and nitrosative stress (IO&NS) pathways, including tryptophan catabolite (TRYCAT), autoimmune, and gut-brain pathways. IO&NS pathways are similarly integral to the pathogenesis of inflammatory bowel disease (IBD). The increased depression prevalence in IBD associates with a lower quality of life and increased morbidity in IBD, highlighting the role of depression in modulating the pathophysiology of IBD.This review covers data within such a wider conceptualization that better explains the heightened co-occurrence of IBD and depression. Common IO&NS underpinning between both disorders is evidenced by increased pro-inflammatory cytokine levels, eg, interleukin-1 (IL-1) and tumor necrosis factor-α, IL-6 trans-signalling; Th-1- and Th-17-like responses; neopterin and soluble IL-2 receptor levels; positive acute phase reactants (haptoglobin and C-reactive protein); lowered levels of negative acute phase reactants (albumin, transferrin, zinc) and anti-inflammatory cytokines (IL-10 and transforming growth factor-β); increased O&NS with damage to lipids, proteinsm and DNA; increased production of nitric oxide (NO) and inducible NO synthase; lowered plasma tryptophan but increased TRYCAT levels; autoimmune responses; and increased bacterial translocation. As such, heightened IO&NS processes in depression overlap with the biological underpinnings of IBD, potentially explaining their increased co-occurrence. This supports the perspective that there is a spectrum of IO&NS disorders that includes depression, both as an emergent comorbidity and as a contributor to IO&NS processes. Such a frame of reference has treatment implications for IBD when "comorbid" with depression.
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Gastrodin ameliorates depressive-like behaviors via modulating gut microbiota in CUMS-induced mice.
PURPOSE: Depression is a psychiatric disorder and the treatment of depression is an urgent problem that need to be solved. Gastrodin (GAS) is a Traditional Chinese Medicine from an orchid and is used for neurological diseases, including depressive disorders. METHODS: To assess the effect of GAS on gut microbiota of depressive mice, we established a chronic unpredictable mild stress (CUMS)-induced mouse model, and GAS was administered to one group of the mice. Animal behavior experiments were used to detect depressive-like behaviors, and 16 S rRNA gene analysis was applied to detect the gut microbiota of each group. All raw sequences were deposited in the NCBI Sequence Read Archive under accession number SRP491061. RESULTS: GAS treatment significantly improved depressive-like behaviors as well as the diversity and abundance of the gut microbiota. The depressive-like behaviors of the CUMS-GAS group were improved in different degrees compared with the CUMS group. The linear discriminant analysis (LDA) of the gut microbiota showed that the makeup of the gut microbiota in mice changed dramatically in the CUMS-GAS group, compared with the CUMS group, Bacteroides (LDA = 3.94, P < 0.05) were enriched in the CUMS-GAS group at the genus level. In comparison to the CUMS group, the CUMS-GAS group had a greater concentration numbers of Lactobacillus, Corynebacterium, Staphylococcus, Bacteroides, Psychrobacter, and Alistipes. CONCLUSION: Our results suggested that GAS improved depressive-like behaviors in mice and impacted the microbial composition of the gut. Our research indicated that dysbiosis of the gut microbiota may be affected by GAS treatment, which improved depressive-like behaviors in the CUMS-induced mouse model of depression.