Depression is a complex and heterogeneous disorder that results from a combination of genetic vulnerability, environmental stressors, and dysregulated biological processes. While systemic inflammation and gut dysbiosis have been extensively investigated in the context of depression, the role of the oral microbiome has only recently begun to emerge. The oral microbiome is a highly diverse and dynamic ecosystem, comprising bacteria, fungi, viruses, and archaea, which coexist in a delicate balance with the host's immune system. This microbial community plays a fundamental role in maintaining not only oral health, but also systemic homeostasis. Emerging evidence suggests that disruptions in this balance, or oral dysbiosis, may contribute to a range of systemic inflammatory conditions, including psychiatric disorders such as depression. Factors comprising periodontal disease, dental infections, and poor oral hygiene can lead to an imbalance in oral microbial composition, promoting immune system activation, chronic inflammation and microbial translocation, which are increasingly recognised mechanisms involved in the pathophysiology of depression. This review delves into the emerging evidence linking oral dysbiosis to depression, elucidating the underlying biological mechanisms and their clinical implications. By bridging the gap between oral health and mental well-being, it underscores the importance of a multidisciplinary approach in addressing depression—one that extends beyond conventional psychiatric treatments to include oral health interventions as a viable component of comprehensive care strategies.
{"title":"From gums to moods: Exploring the impact of the oral microbiota on depression","authors":"Claudio Singh Solorzano , Floriana De Cillis , Elisa Mombelli , Samantha Saleri , Moira Marizzoni , Annamaria Cattaneo","doi":"10.1016/j.bbih.2025.101057","DOIUrl":"10.1016/j.bbih.2025.101057","url":null,"abstract":"<div><div>Depression is a complex and heterogeneous disorder that results from a combination of genetic vulnerability, environmental stressors, and dysregulated biological processes. While systemic inflammation and gut dysbiosis have been extensively investigated in the context of depression, the role of the oral microbiome has only recently begun to emerge. The oral microbiome is a highly diverse and dynamic ecosystem, comprising bacteria, fungi, viruses, and archaea, which coexist in a delicate balance with the host's immune system. This microbial community plays a fundamental role in maintaining not only oral health, but also systemic homeostasis. Emerging evidence suggests that disruptions in this balance, or oral dysbiosis, may contribute to a range of systemic inflammatory conditions, including psychiatric disorders such as depression. Factors comprising periodontal disease, dental infections, and poor oral hygiene can lead to an imbalance in oral microbial composition, promoting immune system activation, chronic inflammation and microbial translocation, which are increasingly recognised mechanisms involved in the pathophysiology of depression. This review delves into the emerging evidence linking oral dysbiosis to depression, elucidating the underlying biological mechanisms and their clinical implications. By bridging the gap between oral health and mental well-being, it underscores the importance of a multidisciplinary approach in addressing depression—one that extends beyond conventional psychiatric treatments to include oral health interventions as a viable component of comprehensive care strategies.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101057"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144580011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-04DOI: 10.1016/j.bbih.2025.101055
Samantha Narvaez , Yizhou Ma , Joshua Chiappelli , Hemalatha Sampath , Alia Warner , Peter Kochunov , Giselli Scaini , Anilkumar Pillai , L. Elliot Hong
Patients with schizophrenia spectrum disorders (SSD) have higher risks for early and adult life traumatic events and suffer from a heightened body response to stress and increased inflammatory activities. We hypothesize that in SSD, the effect of stress is associated with prolonged activation of the inflammatory system and causes elevation in immune markers. We examined the effects of childhood trauma and adult stressful life events on a C-reactive protein (CRP) and their combined contribution to cortical thickness thinning in 49 SSD patients and 26 healthy controls. Participants with SSD reported higher levels of childhood trauma (p = 0.015) and lifetime stressful experiences as measured by a Major Life Event scale (p = 0.00005). Participants with SSD had significantly lower cortical thickness in multiple brain regions but showed no significant elevation in the CRP levels. Only childhood trauma appears to have consistent and significant impacts on multiple cortical regions after accounting for age, sex, CRP and disease effects. These findings may point to the disproportional role of childhood stress in impeding early cortical development.
{"title":"Childhood trauma and inflammatory biomarker effects on cortical thinning in schizophrenia spectrum disorders","authors":"Samantha Narvaez , Yizhou Ma , Joshua Chiappelli , Hemalatha Sampath , Alia Warner , Peter Kochunov , Giselli Scaini , Anilkumar Pillai , L. Elliot Hong","doi":"10.1016/j.bbih.2025.101055","DOIUrl":"10.1016/j.bbih.2025.101055","url":null,"abstract":"<div><div>Patients with schizophrenia spectrum disorders (SSD) have higher risks for early and adult life traumatic events and suffer from a heightened body response to stress and increased inflammatory activities. We hypothesize that in SSD, the effect of stress is associated with prolonged activation of the inflammatory system and causes elevation in immune markers. We examined the effects of childhood trauma and adult stressful life events on a C-reactive protein (CRP) and their combined contribution to cortical thickness thinning in 49 SSD patients and 26 healthy controls. Participants with SSD reported higher levels of childhood trauma (p = 0.015) and lifetime stressful experiences as measured by a Major Life Event scale (p = 0.00005). Participants with SSD had significantly lower cortical thickness in multiple brain regions but showed no significant elevation in the CRP levels. Only childhood trauma appears to have consistent and significant impacts on multiple cortical regions after accounting for age, sex, CRP and disease effects. These findings may point to the disproportional role of childhood stress in impeding early cortical development.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101055"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144596806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-04DOI: 10.1016/j.bbih.2025.101050
Charlotte Sørensen , Ilona Dudka , Ana Virel , Ingemar Kåreholt , Leonie JT. Balter , John Axelsson , Grégoria Kalpouzos , Shireen Sindi
Study objectives
Short and long sleep duration as well as poor sleep quality have been linked to higher prevalence of metabolic disorders. However, it is still unclear how diverse sleep variables relate to different metabolic pathways. This study examines how different features of sleep health relate to serum metabolites.
Methods
The study used data from 197 healthy individuals aged 20–79 (Females n = 103) from the IronAge study performed at Karolinska Institutet in Sweden. Sleep variables were assessed with the Karolinska Sleep Questionnaire, where the following variables were computed: sleep duration, sleep debt, midpoint, social jetlag (i.e., the discrepancy between midpoint on free and workdays), napping frequency and sleep quality. Morning fasting blood samples were collected and 1H NMR spectroscopy was utilized for metabolomic analysis. The metabolites were categorized according to their major metabolic pathways: amino acid, lipid, carbohydrate, energy and gut microbiota. Linear regressions were performed to examine the relationship between each sleep variable and metabolite.
Results
Sleep duration, midpoint of sleep on free days, social jetlag and chronotype associated with eight metabolites at a significance level of p<0.01. Notably, midpoint associated with most metabolites spanning multiple pathways. A later midpoint was associated with higher levels of metabolites in the lipid pathway, and lower levels in the amino acid and energy pathway.
Conclusion
These observations indicate that sleep timing features, midpoint and social jetlag, have a stronger relationship with morning metabolism than other sleep health dimensions. Following replication in larger samples, these complex relationships may hold potential for health promotion.
{"title":"Sleep health associations with serum metabolites in healthy adults","authors":"Charlotte Sørensen , Ilona Dudka , Ana Virel , Ingemar Kåreholt , Leonie JT. Balter , John Axelsson , Grégoria Kalpouzos , Shireen Sindi","doi":"10.1016/j.bbih.2025.101050","DOIUrl":"10.1016/j.bbih.2025.101050","url":null,"abstract":"<div><h3>Study objectives</h3><div>Short and long sleep duration as well as poor sleep quality have been linked to higher prevalence of metabolic disorders. However, it is still unclear how diverse sleep variables relate to different metabolic pathways. This study examines how different features of sleep health relate to serum metabolites.</div></div><div><h3>Methods</h3><div>The study used data from 197 healthy individuals aged 20–79 (Females n = 103) from the IronAge study performed at Karolinska Institutet in Sweden. Sleep variables were assessed with the Karolinska Sleep Questionnaire, where the following variables were computed: sleep duration, sleep debt, midpoint, social jetlag (i.e., the discrepancy between midpoint on free and workdays), napping frequency and sleep quality. Morning fasting blood samples were collected and <sup>1</sup>H NMR spectroscopy was utilized for metabolomic analysis. The metabolites were categorized according to their major metabolic pathways: amino acid, lipid, carbohydrate, energy and gut microbiota. Linear regressions were performed to examine the relationship between each sleep variable and metabolite.</div></div><div><h3>Results</h3><div>Sleep duration, midpoint of sleep on free days, social jetlag and chronotype associated with eight metabolites at a significance level of <em>p<0.01</em>. Notably, midpoint associated with most metabolites spanning multiple pathways. A later midpoint was associated with higher levels of metabolites in the lipid pathway, and lower levels in the amino acid and energy pathway.</div></div><div><h3>Conclusion</h3><div>These observations indicate that sleep timing features, <em>midpoint</em> and <em>social jetlag,</em> have a stronger relationship with morning metabolism than other sleep health dimensions. Following replication in larger samples, these complex relationships may hold potential for health promotion.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101050"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144614362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-04DOI: 10.1016/j.bbih.2025.101054
Gustavo Reis Sampaio , Michell Bruno Lago Silva , Denis Melo Soares , Suzana Braga-de-Souza
Epidemiological data show that the use of alcohol and other psychoactive substances is higher among university students when compared with the general population and high school students. The use of psychotropic drugs by students in health courses requires special attention, taking into account that they will be responsible for the health education and care of the population. This study investigates the factors that determine current prevalence of psychoactive substances use among health students, analyses the impact of associated risks and assesses the significance of gender on substance use. A descriptive cross-sectional study was carried out from September 20, 2019 to June 15, 2021, in which students from Biological and Health Sciences at the Federal University of Bahia (UFBA) were the target population. 514 responses were obtained, of which 502 were considered to fulfil the inclusion criteria. The parameters included recreational use of psychoactive substances, both for lifetime use and for use in the last 3 months; the prevalence of alcohol, cannabis and tobacco was the highest in that order. Only alcohol, cannabis and inhalants showed a percentage of individuals at high risk of developing problems. These results indicate the need for local intervention, in order to prevent risky behaviour, damage to mental health and major consequences for society and academic performance.
{"title":"How does psychoactive substance use affect health students? An important local cutout","authors":"Gustavo Reis Sampaio , Michell Bruno Lago Silva , Denis Melo Soares , Suzana Braga-de-Souza","doi":"10.1016/j.bbih.2025.101054","DOIUrl":"10.1016/j.bbih.2025.101054","url":null,"abstract":"<div><div>Epidemiological data show that the use of alcohol and other psychoactive substances is higher among university students when compared with the general population and high school students. The use of psychotropic drugs by students in health courses requires special attention, taking into account that they will be responsible for the health education and care of the population. This study investigates the factors that determine current prevalence of psychoactive substances use among health students, analyses the impact of associated risks and assesses the significance of gender on substance use. A descriptive cross-sectional study was carried out from September 20, 2019 to June 15, 2021, in which students from Biological and Health Sciences at the Federal University of Bahia (UFBA) were the target population. 514 responses were obtained, of which 502 were considered to fulfil the inclusion criteria. The parameters included recreational use of psychoactive substances, both for lifetime use and for use in the last 3 months; the prevalence of alcohol, cannabis and tobacco was the highest in that order. Only alcohol, cannabis and inhalants showed a percentage of individuals at high risk of developing problems. These results indicate the need for local intervention, in order to prevent risky behaviour, damage to mental health and major consequences for society and academic performance.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101054"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144580012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-04DOI: 10.1016/j.bbih.2025.101058
Karen Giménez-Orenga , Justine Pierquin , Joanna Brunel , Benjamin Charvet , Eva Martín-Martínez , Margot Lemarinier , Steven Fried , Alexandre Lucas , Hervé Perron , Elisa Oltra
Post-COVID-19 condition, such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia (FM), are characterized by fatigue, pain, shortness of breath, sleep disturbances, cognitive dysfunction and other symptoms, heavily impacting on patients daily functioning. Moreover, over half of patients end up fulfilling ME/CFS and/or FM clinical criteria after a few months of SARS-CoV-2 infection. Expression of the toxic human endogenous retrovirus (HERV)-W ENV protein can be induced by viral infection and HERV-W detection was correlated with acute COVID-19 severity and found significantly expressed in post-COVID-19 condition. This study shows that HERV-W ENV may also be present in prepandemic cases of ME/CFS, FM or co-diagnosed with both clinical criteria, suggesting viral participation in these chronic diseases. To learn whether associated antiviral mechanisms may also show differing patterns of immunological responses, we measured IgM, IgG, IgA and IgE antibody isotypes against SARS-CoV-2 spike and nucleocapsid antigens, the levels of IL-6, IL-8, IL-10, IFNγ and TNFα cytokines, the level of NfL, a neural damage biomarker, as well as some blood cell markers potentially related with fatigue. Importantly, some of the measured variables showed a capacity to discriminate post-COVID-19 condition cases from all other participants, with 100 % sensitivity and up to 71.9 % specificity providing a new tool for a differential diagnosis between diseases or syndromes with so many overlapping clinical symptoms. Interestingly, the detected markers showed moderate-to-strong correlations with patient symptoms pointing at novel therapeutic opportunities.
{"title":"Blood parameters differentiate post COVID-19 condition from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Fibromyalgia","authors":"Karen Giménez-Orenga , Justine Pierquin , Joanna Brunel , Benjamin Charvet , Eva Martín-Martínez , Margot Lemarinier , Steven Fried , Alexandre Lucas , Hervé Perron , Elisa Oltra","doi":"10.1016/j.bbih.2025.101058","DOIUrl":"10.1016/j.bbih.2025.101058","url":null,"abstract":"<div><div>Post-COVID-19 condition, such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia (FM), are characterized by fatigue, pain, shortness of breath, sleep disturbances, cognitive dysfunction and other symptoms, heavily impacting on patients daily functioning. Moreover, over half of patients end up fulfilling ME/CFS and/or FM clinical criteria after a few months of SARS-CoV-2 infection. Expression of the toxic human endogenous retrovirus (HERV)-W ENV protein can be induced by viral infection and HERV-W detection was correlated with acute COVID-19 severity and found significantly expressed in post-COVID-19 condition. This study shows that HERV-W ENV may also be present in prepandemic cases of ME/CFS, FM or co-diagnosed with both clinical criteria, suggesting viral participation in these chronic diseases. To learn whether associated antiviral mechanisms may also show differing patterns of immunological responses, we measured IgM, IgG, IgA and IgE antibody isotypes against SARS-CoV-2 spike and nucleocapsid antigens, the levels of IL-6, IL-8, IL-10, IFNγ and TNFα cytokines, the level of NfL, a neural damage biomarker, as well as some blood cell markers potentially related with fatigue. Importantly, some of the measured variables showed a capacity to discriminate post-COVID-19 condition cases from all other participants, with 100 % sensitivity and up to 71.9 % specificity providing a new tool for a differential diagnosis between diseases or syndromes with so many overlapping clinical symptoms. Interestingly, the detected markers showed moderate-to-strong correlations with patient symptoms pointing at novel therapeutic opportunities.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101058"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-04DOI: 10.1016/j.bbih.2025.101052
Nur Hani Zainal
Aims
Major depressive disorder (MDD) is a prevalent mental disorder, and low social support and high strain could impact its long-term symptom severity. Increased inflammation, marked by C-reactive protein (CRP) and fibrinogen, has also been correlated with more MDD symptoms. However, the inflammation-MDD symptom association might vary by social support dimensions. The current study thus examined how social support dimensions moderated the inflammation-MDD severity correlation.
Methods
Community adults (N = 1,054) with and without MDD provided plasma samples to measure CRP and fibrinogen levels and completed self-reports of perceived support and strain from family, friends, and partners at Wave 1 (W1). MDD severity was assessed at W1 and Wave 2 (W2, nine-year follow-up). Multiple linear regressions and generalized additive modeling (GAM) assessed how W1 social support dimensions and inflammation levels interacted to predict W2 MDD severity, controlling for clinical and sociodemographic covariates.
Results
Increased W1 fibrinogen predicted higher W2 MDD severity in participants with lower (vs. higher) W1 social support and higher (vs. lower) social strain (|standardized β| = 0.18–2.31 vs. 0.01–0.03). Further, increased CRP predicted more MDD symptoms in participants with higher (vs. lower) social strain (|β| = 0.24–0.26 vs. 0.15–0.16). These significant interaction findings were identical in linear and GAM models that accommodate non-linear associations. Conclusions: Results suggested that increased proinflammatory activity indexed by CRP and fibrinogen levels could predict nine-year MDD severity under social strains, consistent with the social signal transduction theory. Improving social support and decreasing social strain might buffer inflammation-related depression.
目的重度抑郁症（MDD）是一种常见的精神障碍，低社会支持和高压力会影响其长期症状的严重程度。以c反应蛋白（CRP）和纤维蛋白原为标志的炎症增加也与更多的重度抑郁症症状相关。然而，炎症与重度抑郁症症状的关联可能因社会支持维度而异。因此，目前的研究检验了社会支持维度如何调节炎症与重度抑郁症严重程度的相关性。方法社区成人（N = 1,054）有或没有重度抑郁症，提供血浆样本测量CRP和纤维蛋白原水平，并在第1波（W1）完成来自家人、朋友和伴侣的感知支持和压力的自我报告。在W1和第二阶段（W2, 9年随访）评估重度抑郁症的严重程度。多元线性回归和广义加性建模（GAM）评估了W1社会支持维度和炎症水平如何相互作用，以预测W2 MDD严重程度，控制了临床和社会人口统计学协变量。结果W1纤维蛋白原升高预示着W1社会支持较低（vs.较高）和社会压力较高（vs.较低）的参与者W2 MDD严重程度较高（|标准化β| = 0.18-2.31 vs. 0.01-0.03）。此外，在社交压力较高（相对较低）的参与者中，CRP升高预示着更多的重度抑郁症症状（|β| = 0.24-0.26 vs 0.15-0.16）。这些重要的相互作用结果在线性和GAM模型中是相同的，以适应非线性关联。结论：以CRP和纤维蛋白原水平为指标的促炎活性升高可以预测社会压力下9年MDD严重程度，与社会信号转导理论一致。改善社会支持和减少社会压力可能会缓解炎症相关的抑郁症。
{"title":"The inflammation-depression link: How social networks buffer or exacerbate risk","authors":"Nur Hani Zainal","doi":"10.1016/j.bbih.2025.101052","DOIUrl":"10.1016/j.bbih.2025.101052","url":null,"abstract":"<div><h3>Aims</h3><div>Major depressive disorder (MDD) is a prevalent mental disorder, and low social support and high strain could impact its long-term symptom severity. Increased inflammation, marked by C-reactive protein (CRP) and fibrinogen, has also been correlated with more MDD symptoms. However, the inflammation-MDD symptom association might vary by social support dimensions. The current study thus examined how social support dimensions moderated the inflammation-MDD severity correlation.</div></div><div><h3>Methods</h3><div>Community adults (<em>N</em> = 1,054) with and without MDD provided plasma samples to measure CRP and fibrinogen levels and completed self-reports of perceived support and strain from family, friends, and partners at Wave 1 (W1). MDD severity was assessed at W1 and Wave 2 (W2, nine-year follow-up). Multiple linear regressions and generalized additive modeling (GAM) assessed how W1 social support dimensions and inflammation levels interacted to predict W2 MDD severity, controlling for clinical and sociodemographic covariates.</div></div><div><h3>Results</h3><div>Increased W1 fibrinogen predicted higher W2 MDD severity in participants with lower (vs. higher) W1 social support and higher (vs. lower) social strain (|standardized β| = 0.18–2.31 vs. 0.01–0.03). Further, increased CRP predicted more MDD symptoms in participants with higher (vs. lower) social strain (|β| = 0.24–0.26 vs. 0.15–0.16). These significant interaction findings were identical in linear and GAM models that accommodate non-linear associations. <strong>Conclusions</strong>: Results suggested that increased proinflammatory activity indexed by CRP and fibrinogen levels could predict nine-year MDD severity under social strains, consistent with the social signal transduction theory. Improving social support and decreasing social strain might buffer inflammation-related depression.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101052"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144605251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-04DOI: 10.1016/j.bbih.2025.101049
Sara Alaeddin , Anushka Chatterjee , Tara L. Roberts , Genevieve Z. Steiner-Lim , Slade O. Jensen , Erika Gyengesi , Gerald Muench , Vincent Ho
Faecal Microbiota Transplantation (FMT) is a widely used microbiota-modulation technique to treat recurrent Clostridioides difficile infections (rCDI). Rodent studies and clinical trials on probiotic interventions indicate that alterations in microbiota composition may impact cognitive function. To explore whether FMT influences cognitive function in humans, we conducted a systematic search and narrative synthesis and identified 14 studies examining its effects on cognition. A variety of cohort studies, single-arm trials, case reports and randomised, placebo-controlled trials have been conducted on different neurological patient cohorts, including those with Hepatic Encephalopathy, Parkinson's Disease, dementia, and Mild Cognitive Impairment. FMT has been shown to have a significant impact on cognitive function in these populations, accompanied by alterations in microbial composition and blood markers. Interestingly, success was influenced by the route of FMT administration, indicating greater efficacy of rectal cf. oral administration on microbiome composition and cognitive improvements. However, no clinical trials have yet examined the effects of FMT on cognitively healthy individuals. FMT appears to have potential as a therapeutic strategy for cognitive impairment, though further research with larger sample sizes is needed to explore its effects in both impaired and cognitively healthy populations.
{"title":"Exploring the effects of faecal microbiota transplantation on cognitive function: A review of clinical trials","authors":"Sara Alaeddin , Anushka Chatterjee , Tara L. Roberts , Genevieve Z. Steiner-Lim , Slade O. Jensen , Erika Gyengesi , Gerald Muench , Vincent Ho","doi":"10.1016/j.bbih.2025.101049","DOIUrl":"10.1016/j.bbih.2025.101049","url":null,"abstract":"<div><div>Faecal Microbiota Transplantation (FMT) is a widely used microbiota-modulation technique to treat recurrent <em>Clostridioides difficile</em> infections (rCDI). Rodent studies and clinical trials on probiotic interventions indicate that alterations in microbiota composition may impact cognitive function. To explore whether FMT influences cognitive function in humans, we conducted a systematic search and narrative synthesis and identified 14 studies examining its effects on cognition. A variety of cohort studies, single-arm trials, case reports and randomised, placebo-controlled trials have been conducted on different neurological patient cohorts, including those with Hepatic Encephalopathy, Parkinson's Disease, dementia, and Mild Cognitive Impairment. FMT has been shown to have a significant impact on cognitive function in these populations, accompanied by alterations in microbial composition and blood markers. Interestingly, success was influenced by the route of FMT administration, indicating greater efficacy of rectal cf. oral administration on microbiome composition and cognitive improvements. However, no clinical trials have yet examined the effects of FMT on cognitively healthy individuals. FMT appears to have potential as a therapeutic strategy for cognitive impairment, though further research with larger sample sizes is needed to explore its effects in both impaired and cognitively healthy populations.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101049"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144571408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-04DOI: 10.1016/j.bbih.2025.101053
Zaiming Liao , Sheng Guo , Kunying Wang , Yanmin Xu , Rui Zheng , Binhe Yu , Guoan Zhao , Ruizhi Zhang , Xiaohong Kang , Sizhi Ai
Backgrounds
Observational research has shown significant associations between inflammatory factors and sleep. Experimental studies suggested acute increase in the levels of inflammatory markers following sleep deprivation and sleep restriction. However, the causal association between inflammatory factors and sleep remains unclear in chronic and natural settings.
Objectives
This study aimed to investigate the causal association of inflammatory factors with chronotype, daytime napping, daytime sleepiness, insomnia symptoms, and sleep duration.
Methods
Two-sample bidirectional Mendelian randomization (MR) analysis was employed to investigate the causal associations between 91 inflammatory factors and 7 sleep-related traits. Summary-level data of inflammatory factors were derived from the EBI GWAS Catalog (n = 14,824); sleep-related traits were obtained from UK Biobank. We calculated effect estimates using the inverse-variance weighted (IVW), weighted median, and MR-Egger methods. Heterogeneity and pleiotropy were detected and measured by the MR pleiotropy residual sum and outlier, Cochran's Q statistics, and MR-Egger regression.
Results
Significant bidirectional causal associations were observed. The most crucial findings included the causal effects of CD40 (OR = 1.02, 95 % CI: 1.01–1.03), ST1A1 (OR = 0.97, 95 % CI: 0.96–0.99), uPA (OR = 1.03, 95 % CI: 1.01–1.04) on chronotype, and FGF-21 (OR = 1.02, 95 % CI: 1.01–1.03), hGDNF (OR = 1.01, 95 % CI: 1.00–1.02), TNFB (OR = 0.99, 95 % CI: 0.98–1.00), TNFSF14 (OR = 1.01, 95 % CI: 1.00–1.02) on napping. Overall, 30 inflammatory factors were found to causally affect sleep traits, and 20 reciprocal effects were observed.
Conclusion
Our study suggested a bidirectional causal association between inflammatory factors and sleep-related traits, such as the roles of CD40, ST1A1, and uPA in regulating chronotype, and FGF-21, hGDNF, and TNFB in influencing daytime napping.
{"title":"Bidirectional Mendelian randomization analysis of inflammatory factors and sleep related traits","authors":"Zaiming Liao , Sheng Guo , Kunying Wang , Yanmin Xu , Rui Zheng , Binhe Yu , Guoan Zhao , Ruizhi Zhang , Xiaohong Kang , Sizhi Ai","doi":"10.1016/j.bbih.2025.101053","DOIUrl":"10.1016/j.bbih.2025.101053","url":null,"abstract":"<div><h3>Backgrounds</h3><div>Observational research has shown significant associations between inflammatory factors and sleep. Experimental studies suggested acute increase in the levels of inflammatory markers following sleep deprivation and sleep restriction. However, the causal association between inflammatory factors and sleep remains unclear in chronic and natural settings.</div></div><div><h3>Objectives</h3><div>This study aimed to investigate the causal association of inflammatory factors with chronotype, daytime napping, daytime sleepiness, insomnia symptoms, and sleep duration.</div></div><div><h3>Methods</h3><div>Two-sample bidirectional Mendelian randomization (MR) analysis was employed to investigate the causal associations between 91 inflammatory factors and 7 sleep-related traits. Summary-level data of inflammatory factors were derived from the EBI GWAS Catalog (n = 14,824); sleep-related traits were obtained from UK Biobank. We calculated effect estimates using the inverse-variance weighted (IVW), weighted median, and MR-Egger methods. Heterogeneity and pleiotropy were detected and measured by the MR pleiotropy residual sum and outlier, Cochran's Q statistics, and MR-Egger regression.</div></div><div><h3>Results</h3><div>Significant bidirectional causal associations were observed. The most crucial findings included the causal effects of CD40 (OR = 1.02, 95 % CI: 1.01–1.03), ST1A1 (OR = 0.97, 95 % CI: 0.96–0.99), uPA (OR = 1.03, 95 % CI: 1.01–1.04) on chronotype, and FGF-21 (OR = 1.02, 95 % CI: 1.01–1.03), hGDNF (OR = 1.01, 95 % CI: 1.00–1.02), TNFB (OR = 0.99, 95 % CI: 0.98–1.00), TNFSF14 (OR = 1.01, 95 % CI: 1.00–1.02) on napping. Overall, 30 inflammatory factors were found to causally affect sleep traits, and 20 reciprocal effects were observed.</div></div><div><h3>Conclusion</h3><div>Our study suggested a bidirectional causal association between inflammatory factors and sleep-related traits, such as the roles of CD40, ST1A1, and uPA in regulating chronotype, and FGF-21, hGDNF, and TNFB in influencing daytime napping.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101053"},"PeriodicalIF":3.7,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144563252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-30DOI: 10.1016/j.bbih.2025.101048
Leonard B. Weinstock , Lawrence B. Afrin , Angela M. Reiersen , Jill Brook , Svetlana Blitshteyn , Gillian Ehrlich , Jill R. Schofield , Laurence Kinsella , David Kaufman , Tania Dempsey , Gerhard J. Molderings
Background
Neuropsychiatric disorders have been observed in mast cell activation syndrome (MCAS). MCAS is a common, yet rarely diagnosed, inflammatory, and immunologic disease characterized by mast cell dysregulation.
Methods
Questionnaires from 553 MCAS and 558 control subjects determined the prevalence and odds ratio of neurologic disorders (fatigue, cognitive dysfunction, fainting/near fainting, migraine-like headaches, muscle pain/tenderness/weakness, pain/numbness/tingling in extremities, restless legs syndrome, seizure-like activity, insomnia, sleep attacks, tinnitus, acoustic startle, Tourette's syndrome, resting tremor, and light/sun/pain/odors/scents/noise hypersensitivity) and psychiatric disorders (anxiety, agoraphobia, panic attacks, depression, bipolar depression, mania/hypomania, psychosis/schizophrenia, hallucinations, obsessive compulsive disorder, attention-deficit/hyperactivity disorder, anger management problems, post-traumatic stress disorder, suicidal thoughts, and eating disorders).
Results
Among 19 neurologic disorders, female MCAS patients reported higher rates in all but 1 disorder and male MCAS patients reported higher rates in all but 2 disorders. Among 14 psychiatric disorders, female MCAS patients reported higher rates in all and male MCAS patients reported higher rates in 8 disorders. Many of the disorders with increased prevalences were statistically greater compared to corresponding controls.
In self-reported ratings for effects on health status (0 = no benefit, 10 = maximum benefit), mean (SD) response was 6.3 (2.5) for antihistamines, 5.6 (3.2) for low-dose naltrexone, and 5.6 (3.1) for benzodiazepines.
Conclusion
MCAS subjects have significantly elevated odds ratios for many neuropsychiatric disorders and may see improvement of symptoms using MCAS-targeted therapies, suggesting that mast cell dysregulation affects the brain and peripheral nervous systems and contributes to neuropsychiatric symptoms. Certain mast cell mediators, specific genetic predisposition, and life experiences could determine which disorder is apt to develop or worsen.
{"title":"Prevalence and treatment response of neuropsychiatric disorders in mast cell activation syndrome","authors":"Leonard B. Weinstock , Lawrence B. Afrin , Angela M. Reiersen , Jill Brook , Svetlana Blitshteyn , Gillian Ehrlich , Jill R. Schofield , Laurence Kinsella , David Kaufman , Tania Dempsey , Gerhard J. Molderings","doi":"10.1016/j.bbih.2025.101048","DOIUrl":"10.1016/j.bbih.2025.101048","url":null,"abstract":"<div><h3>Background</h3><div>Neuropsychiatric disorders have been observed in mast cell activation syndrome (MCAS). MCAS is a common, yet rarely diagnosed, inflammatory, and immunologic disease characterized by mast cell dysregulation.</div></div><div><h3>Methods</h3><div>Questionnaires from 553 MCAS and 558 control subjects determined the prevalence and odds ratio of neurologic disorders (fatigue, cognitive dysfunction, fainting/near fainting, migraine-like headaches, muscle pain/tenderness/weakness, pain/numbness/tingling in extremities, restless legs syndrome, seizure-like activity, insomnia, sleep attacks, tinnitus, acoustic startle, Tourette's syndrome, resting tremor, and light/sun/pain/odors/scents/noise hypersensitivity) and psychiatric disorders (anxiety, agoraphobia, panic attacks, depression, bipolar depression, mania/hypomania, psychosis/schizophrenia, hallucinations, obsessive compulsive disorder, attention-deficit/hyperactivity disorder, anger management problems, post-traumatic stress disorder, suicidal thoughts, and eating disorders).</div></div><div><h3>Results</h3><div>Among 19 neurologic disorders, female MCAS patients reported higher rates in all but 1 disorder and male MCAS patients reported higher rates in all but 2 disorders. Among 14 psychiatric disorders, female MCAS patients reported higher rates in all and male MCAS patients reported higher rates in 8 disorders. Many of the disorders with increased prevalences were statistically greater compared to corresponding controls.</div><div>In self-reported ratings for effects on health status (0 = no benefit, 10 = maximum benefit), mean (SD) response was 6.3 (2.5) for antihistamines, 5.6 (3.2) for low-dose naltrexone, and 5.6 (3.1) for benzodiazepines.</div></div><div><h3>Conclusion</h3><div>MCAS subjects have significantly elevated odds ratios for many neuropsychiatric disorders and may see improvement of symptoms using MCAS-targeted therapies, suggesting that mast cell dysregulation affects the brain and peripheral nervous systems and contributes to neuropsychiatric symptoms. Certain mast cell mediators, specific genetic predisposition, and life experiences could determine which disorder is apt to develop or worsen.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101048"},"PeriodicalIF":3.7,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144549718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-30DOI: 10.1016/j.bbih.2025.101046
Sean Daniel , Ruihua Hou , Ian Galea , Diederik Bulters
Background
Subarachnoid haemorrhage (SAH) is a severe type of intracranial bleed that causes significant morbidity. One of the most overlooked yet commonly reported symptom is persistent fatigue. Fatigue in the general population has been associated with inflammation and elevated C-reactive protein (CRP). Since inflammation and raised CRP are observed post-SAH, we hypothesized that CRP is associated with fatigue severity after SAH.
Methods
Data from 95 patients (26 males, 69 females; mean age 56 years) previously recruited to the SAS trial, a prospective randomised controlled trial (2016–2019) investigating the efficacy of sulforaphane after SAH, were analyzed. In this study CRP was measured on days 1, 7, and 28 post-SAH, and fatigue severity assessed using the Short-Form Health Survey (SF-36) on days 28, 90, and 180. Multivariable regression was conducted controlling for confounders, including age, gender, initial volume of blood on CT and World Federation of Neurological Surgeons (WFNS) grade.
Results
There was a robust association between the severity of fatigue at day 28 and CRP levels at baseline (OR = -2.67 (−1.23 to −0.18), p = 0.001) and CRP on day 28 (OR = -2.56 (−1.01 to −0.12), p = 0.013), even after controlling for confounders including blood volume and WFNS. There was no suggestion of an association between day 7 CRP and fatigue on day 28 (OR = -1.07 (−0.82 to 0.25), p = 0.287). There were no associations with any other fatigue timepoints.
Conclusion
CRP and fatigue in SAH patients are associated. The timings of the associations of baseline and day 28 CRP (but not day 7) with day 28 fatigue, and their independence from bleed severity suggest that fatigue is related partly to the magnitude of the initial response to the SAH and partly due to the degree of ongoing response at day 28 but not due to other events occurring in between. The lack of association of early CRP with fatigue beyond day 28 suggests that later fatigue is not driven by the initial CRP-related response to SAH. Further studies are needed to examine later CRP and the determinants of persistent fatigue.
{"title":"C-reactive protein and fatigue after subarachnoid haemorrhage","authors":"Sean Daniel , Ruihua Hou , Ian Galea , Diederik Bulters","doi":"10.1016/j.bbih.2025.101046","DOIUrl":"10.1016/j.bbih.2025.101046","url":null,"abstract":"<div><h3>Background</h3><div>Subarachnoid haemorrhage (SAH) is a severe type of intracranial bleed that causes significant morbidity. One of the most overlooked yet commonly reported symptom is persistent fatigue. Fatigue in the general population has been associated with inflammation and elevated C-reactive protein (CRP). Since inflammation and raised CRP are observed post-SAH, we hypothesized that CRP is associated with fatigue severity after SAH.</div></div><div><h3>Methods</h3><div>Data from 95 patients (26 males, 69 females; mean age 56 years) previously recruited to the SAS trial, a prospective randomised controlled trial (2016–2019) investigating the efficacy of sulforaphane after SAH, were analyzed. In this study CRP was measured on days 1, 7, and 28 post-SAH, and fatigue severity assessed using the Short-Form Health Survey (SF-36) on days 28, 90, and 180. Multivariable regression was conducted controlling for confounders, including age, gender, initial volume of blood on CT and World Federation of Neurological Surgeons (WFNS) grade.</div></div><div><h3>Results</h3><div>There was a robust association between the severity of fatigue at day 28 and CRP levels at baseline (OR = -2.67 (−1.23 to −0.18), p = 0.001) and CRP on day 28 (OR = -2.56 (−1.01 to −0.12), p = 0.013), even after controlling for confounders including blood volume and WFNS. There was no suggestion of an association between day 7 CRP and fatigue on day 28 (OR = -1.07 (−0.82 to 0.25), p = 0.287). There were no associations with any other fatigue timepoints.</div></div><div><h3>Conclusion</h3><div>CRP and fatigue in SAH patients are associated. The timings of the associations of baseline and day 28 CRP (but not day 7) with day 28 fatigue, and their independence from bleed severity suggest that fatigue is related partly to the magnitude of the initial response to the SAH and partly due to the degree of ongoing response at day 28 but not due to other events occurring in between. The lack of association of early CRP with fatigue beyond day 28 suggests that later fatigue is not driven by the initial CRP-related response to SAH. Further studies are needed to examine later CRP and the determinants of persistent fatigue.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101046"},"PeriodicalIF":3.7,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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