Brain, behavior, & immunity - health最新文献

{"title":"Social inhibition in depressed patients is associated with an altered activation profile of the interleukin-6-inducible transcription factor STAT3","authors":"Katharina von Knebel ,&nbsp;Julia Staab ,&nbsp;Anke Gregus ,&nbsp;Linus Remling ,&nbsp;Oliver Wirths ,&nbsp;Carsten Spitzer ,&nbsp;Christoph Herrmann-Lingen ,&nbsp;Holger M. Reichardt ,&nbsp;Thomas Meyer","doi":"10.1016/j.bbih.2025.100968","DOIUrl":"10.1016/j.bbih.2025.100968","url":null,"abstract":"<div><h3>Objective</h3><div>Numerous studies have described the role of STAT3 (signal transducer and activator of transcription 3) in infections, but little is known on whether this transcription factor is linked to negative affectivity (NA) and social inhibition (SI), leading to social withdrawal as a typical symptom of various infections.</div></div><div><h3>Methods</h3><div>In this study, we isolated peripheral blood mononuclear cells (PBMCs) from 63 consecutive depressed patients (mean age 41.4 ± 16.1 years; 40 females) before and after psychotherapeutic intervention and measured STAT3 tyrosine phosphorylation (pSTAT3) with and without <em>in vitro</em> interleukin-6 (IL-6) stimulation of these cells using flow cytometry. In addition, all study participants were assessed for NA and SI using the German version of the Type D Scale-14 (DS-14) questionnaire with a cut-off level of ≥10 for each subscale.</div></div><div><h3>Results</h3><div>While NA was unrelated to STAT3 activity, PBMCs from SI-positive patients had an increased baseline STAT3 activation level, which made the cells less sensitive to <em>in vitro</em> IL-6 stimulation (11.5% vs. 9.1%, p = 0.036). The stimulatory capacity, defined as the difference in pSTAT3 levels from IL-6-stimulated to unstimulated cells during hospitalization, was significantly lower in PBMCs from SI-positive than from SI-negative patients (−1.7% vs. 6.6%, p = 0.007). The sensitivity of PBMCs to IL-6 stimulation was negatively correlated with the SI score (r = −0.295, p = 0.019). Of note, the altered sensitivity to STAT3 phosphorylation remained stable, when adjusted for clinically relevant confounders in multivariate analysis (Exp(β) = 0.891, 95%-confidence interval = 0.804–0.988, p = 0.029).</div></div><div><h3>Conclusion</h3><div>These findings point towards a possible relationship between STAT3 signaling and social inhibition in depressed patients.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100968"},"PeriodicalIF":3.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143526827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNAs modulate CaMKIIα/SIRT1 signaling pathway as a biomarker of cognitive ability in adolescents","authors":"Li-Ching Lee ,&nbsp;Ming-Tsan Su ,&nbsp;Lei Bao ,&nbsp;Po-Lei Lee ,&nbsp;Shane Tutwiler ,&nbsp;Ting-Kuang Yeh ,&nbsp;Chun-Yen Chang","doi":"10.1016/j.bbih.2025.100970","DOIUrl":"10.1016/j.bbih.2025.100970","url":null,"abstract":"<div><div>The dynamic regulation of synaptic plasticity underlies memory formation, involving intricate signaling pathways with both facilitatory and inhibitory roles. MicroRNAs are emerging modulators of memory processes through their fine-tuning of gene expression. To explore the influence of miRNAs on adolescent cognitive function, we investigated the association between academic performance, cognitive ability as measured by the Inquiry for Scientific Thinking, Analytics, and Reasoning test, and plasma miRNA profiling in 486 senior high school students. Our analysis identified 38 differentially expressed miRNAs between students with high and low academic performance. Notably, miR-219 b/548e/628/885 and miR-30a/30c-1/195/204 potentially targeted genes associated with the CaMKII/SIRT1 signaling pathway, a crucial facilitator of memory consolidation. Collectively, our findings suggest that specific plasma miRNAs, particularly the CaMKII/SIRT1-related miR-30a/30c-1/195/204 cluster, potentially serve as promising biomarkers for cognitive function in adolescents. Our findings further support the proposed interaction between NF-kB activity and CaMKIIα in regulating synaptic plasticity. Under hypomethylation conditions, increased NF-kB activity, a key component of inflammation and neural plasticity, influences learning and memory. This biological pathway, representing the initiation of epigenetic memory, demonstrates significant predictive power for both cognitive ability and academic performance.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100970"},"PeriodicalIF":3.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143512289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ligature-induced periodontitis in a transgenic mouse model of Alzheimer's disease dysregulates neuroinflammation, exacerbates cognitive impairment, and accelerates amyloid pathology","authors":"Daniela M. Jimenez-Harrison ,&nbsp;Michael J. Butler ,&nbsp;Haanya Ijaz ,&nbsp;Rami Alsabbagh ,&nbsp;Menaz N. Bettes ,&nbsp;James W. DeMarsh ,&nbsp;Sabrina E. Mackey-Alfonso ,&nbsp;Stephanie M. Muscat ,&nbsp;Bryan D. Alvarez ,&nbsp;Jade A. Blackwell ,&nbsp;Ashton Taylor ,&nbsp;Jeferson Jantsch ,&nbsp;Andrew A. Sanchez ,&nbsp;Sarah B. Peters ,&nbsp;Ruth M. Barrientos","doi":"10.1016/j.bbih.2025.100969","DOIUrl":"10.1016/j.bbih.2025.100969","url":null,"abstract":"<div><div>A growing body of literature has identified periodontal disease among the modifiable risk factors for Alzheimer's disease (AD), but the mechanisms underlying this relationship is unknown. This study investigated this relationship using a ligature-induced preclinical periodontitis (Pd) model in non-transgenic (non-Tg) and 3xTg-AD mice. We found that ligature placement caused significant alveolar bone loss, with 3xTg-AD mice exhibiting exacerbated bone loss, suggesting AD-related genetic risk may amplify disease progression. Pd induced robust <em>local</em> inflammatory gene expression in both genotypes, but 3xTg-AD mice indicated a dysregulated immune response. Cognitive deficits were observed only in Pd-afflicted 3xTg-AD mice, specifically in hippocampus-mediated spatial memory and perirhinal cortex-mediated object recognition memory, while non-Tg mice remained unaffected. Neuroinflammatory responses varied by brain region, with the hippocampus and prefrontal cortex (PFC) showing the most pronounced changes. In these regions, 3xTg-AD mice exhibited significantly altered cytokine gene expression compared to non-Tg mice, particularly at later time points. Synaptic markers revealed vulnerabilities in 3xTg-AD mice, including reduced baseline <em>Syp</em> expression and dysregulated <em>Synpo</em> post-ligature. Pd transiently reduced glutamate receptor gene expression in both genotypes, with non-Tg mice showing persistent changes, potentially linked to preserved memory. Pd also accelerated amyloid-β (Aβ) deposition and sustained neurodegeneration in 3xTg-AD mice. Overall, this study shows that combining Pd and AD-related genetic risk exacerbates inflammation, cognitive impairment, synaptic dysfunction, Aβ pathology, and neurodegeneration. Neither insult alone was sufficient to produce these effects, highlighting the synergistic impact. These findings emphasize the need to explore anti-inflammatory interventions and downstream mechanisms to mitigate the confluence of these diseases.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100969"},"PeriodicalIF":3.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143488785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk factors for fatigue severity in the post-COVID-19 condition: A prospective controlled cohort study of nonhospitalised adolescents and young adults","authors":"Joel Selvakumar ,&nbsp;Lise Beier Havdal ,&nbsp;Elias Myrstad Brodwall ,&nbsp;Silke Sommen ,&nbsp;Lise Lund Berven ,&nbsp;Tonje Stiansen-Sonerud ,&nbsp;Erin Cvejic ,&nbsp;Vegard Bruun Bratholm Wyller","doi":"10.1016/j.bbih.2025.100967","DOIUrl":"10.1016/j.bbih.2025.100967","url":null,"abstract":"<div><div>Long COVID is a global health concern, leading to persistent symptoms and disability long after the acute SARS-CoV-2 infection in most age groups. The condition can manifest even following mild COVID-19, and in young people, it may have serious adverse consequences for educational attainment and transition to adulthood. Fatigue is the most prevalent symptom, but the underlying mechanisms remain poorly understood. In this prospective study of 404 SARS-CoV-2-positive and 105 SARS-CoV-2 negative, non-hospitalised youth (ages 12–25, female 62%), we investigated which factors in the early convalescent stage (&lt;28 days since test) were associated with the severity of persistent fatigue at 6 months after infection. Participants completed questionnaires regarding clinical symptoms, social factors and psychological traits, and were subject to clinical and functional testing and biomarker analyses. Variables with significant (p &lt; 0.2) associations to the outcome in simple linear regression were chosen for multivariable modelling, together with potential confounders. In the final multivariable model, SARS-CoV-2-positivity was a minor risk factor for fatigue severity at six months. Baseline severity of symptoms was the main risk factor and correlated with psychosocial factors such as loneliness and neuroticism, rather than biomarkers. Our results suggest that factors not related to infection are major risk factors for persistent fatigue in this age group.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100967"},"PeriodicalIF":3.7,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143478922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Specific immune-inflammatory profiles and neurocognitive deficits predict illness trajectories in people with type 2 diabetes mellitus or psychiatric disorders","authors":"Joan Vicent Sánchez-Ortí ,&nbsp;Patricia Correa-Ghisays ,&nbsp;Vicent Balanzá-Martínez ,&nbsp;Gabriel Selva-Vera ,&nbsp;Víctor M. Victor ,&nbsp;Constanza San Martin Valenzuela ,&nbsp;Pau Soldevila-Matías ,&nbsp;Fabián Robledo-Yagüe ,&nbsp;María Flores-Rodero ,&nbsp;Jon Sánchez-Valle ,&nbsp;Jaume Forés-Martos ,&nbsp;Diego Macías Saint-Gerons ,&nbsp;Inmaculada Fuentes-Durá ,&nbsp;Rafael Tabarés-Seisdedos","doi":"10.1016/j.bbih.2025.100962","DOIUrl":"10.1016/j.bbih.2025.100962","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;div&gt;Psychiatric disorders and type 2 diabetes mellitus (T2DM) are chronic conditions that are often comorbid with each other. Neurocognitive and functional impairments are associated with numerous clinical changes during the course of illness. Immune-inflammatory dysfunction is emerging as a critical factor in the progression of these disorders. This study aimed to identify neurocognitive deficits and immune-inflammatory biomarkers that are suitable for signaling different illness trajectories from transdiagnostic and longitudinal perspectives.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Clinical status, neurocognitive and functional performance, and peripheral blood biomarkers of immune-inflammation were assessed twice a year in 165 individuals, including 30 with schizophrenia (SZ), 42 with bipolar disorder (BD), 35 with major depressive disorder (MDD), 30 with T2DM, and 28 healthy controls (HCs). Participants with chronic illness (n = 137) were stratified into quartiles, taking their years of illness duration at baseline as a reference into categories of short illness duration (SD; n = 37), middle illness duration (MD; n = 36), long illness duration (LD; n = 32), and very long illness duration (VLD; n = 32). The illness duration was used to measure the illness trajectory, and the exposure of interest was clinical progression, calculated as the difference between clinical severity at baseline (T1) and after 1 year (T2).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Neurocognitive impairment was more significant in the VLD group than in the other groups, with small–moderate effect sizes (F = 2.9 to 9.3; p &lt; 0.05−0.0001; η&lt;sup&gt;2&lt;/sup&gt;p = 0.06−0.24). Moreover, the HC group showed significantly higher functional outcomes than the other groups (F = 5.8 to 6.0; p &lt; 0.0001; η&lt;sup&gt;2&lt;/sup&gt;p = 0.13−0.16). On the contrary, the HC group showed lower levels of immune-inflammatory markers (white blood cell count, absolute neutrophils, absolute monocytes, absolute basophiles, neutrophils/lymphocyte ratio, and platelets/lymphocyte ratio [PLR]) (F = 2.9 to 6.7; p &lt; 0.05−0.0001; η&lt;sup&gt;2&lt;/sup&gt;p = 0.07−0.18). In all groups, significant prospective associations were observed between cognitive function (short-term memory and processing speed), global functional scores, immune-inflammatory biomarkers (monocyte/lymphocyte ratio [MLR] and PLR), and clinical status (p &lt; 0.05). Furthermore, a similar combination of neurocognitive deficits and immune-inflammatory alterations compounded the transdiagnostic model that best discriminated the different illness trajectories (χ&lt;sup&gt;2&lt;/sup&gt; = 67.4 to 78.7; p &lt; 0.05−0.01).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Neurocognitive dysfunction and systemic inflammation are associated with prolonged illness trajectories in individuals with psychiatric disorders and T2DM. An immune-inflammatory profile and neurocognitive and functional performance may be valuable to differentiate individuals with different illn","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100962"},"PeriodicalIF":3.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The vagus nerve-dependent lung-brain axis mediates brain demyelination following acute lung injury","authors":"Dan Xu ,&nbsp;Mingming Zhao ,&nbsp;Guilin Liu ,&nbsp;Tingting Zhu ,&nbsp;Yi Cai ,&nbsp;Rumi Murayama ,&nbsp;Yong Yue ,&nbsp;Kenji Hashimoto","doi":"10.1016/j.bbih.2025.100966","DOIUrl":"10.1016/j.bbih.2025.100966","url":null,"abstract":"<div><div>Patients with acute lung injury (ALI) often experience psychiatric and neurological symptoms; however, the precise underlying mechanisms remain unclear. Given that white matter loss (demyelination) contributes to these symptoms, we investigated whether lipopolysaccharide (LPS)-induced ALI leads to brain demyelination via a vagus nerve-dependent lung-brain axis. A single intratracheal injection of LPS caused severe lung injury and demyelination in the corpus callosum (CC) of mouse brains. Subdiaphragmatic vagotomy did not affect LPS-induced lung injury or demyelination in the CC. Interestingly, cervical vagotomy significantly attenuated LPS-induced hypo-locomotion, plasma interleukin-6 levels, and demyelination in the CC of ALI mice without influencing lung injury. These findings demonstrate that ALI can induce demyelination in the CC of the mouse brain via a cervical vagus nerve-dependent lung-brain axis, highlighting the critical role of this pathway in the psychiatric and neurological symptoms observed in ALI patients.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100966"},"PeriodicalIF":3.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preliminary evaluation of a mindfulness intervention program in women with long COVID dysautonomia symptoms","authors":"Elizabeth Vandenbogaart ,&nbsp;Matthew Figueroa ,&nbsp;Diana Winston ,&nbsp;Steve Cole ,&nbsp;Julienne Bower ,&nbsp;Jeffrey J. Hsu","doi":"10.1016/j.bbih.2025.100963","DOIUrl":"10.1016/j.bbih.2025.100963","url":null,"abstract":"<div><h3>Background</h3><div>The symptom burden for patients with Long COVID-associated dysautonomia is high, yet there are currently no effective treatments. Mindfulness programs reduce psychological and physical symptoms as well as inflammatory gene expression in a variety of medical conditions. The study aim was to evaluate the effect of a six-week mindfulness program in women with Long COVID dysautonomia symptoms.</div></div><div><h3>Methods</h3><div>Using a single arm, pre- and posttest design, women aged 18–54 years with Long COVID and orthostatic intolerance suggestive of dysautonomia were recruited from a single center. Participants attended a standardized, six-week, virtual mindfulness program. An active stand test and 6-min walk test (6MWT) were performed at baseline and post-intervention. Self-reported measures of physical and mental health symptoms collected at baseline, post-intervention and 4 week follow up included the composite autonomic symptom score (COMPASS-31), perceived stress (PSS), anxiety (GAD7), depression (PHQ8), COVID-19 event specific distress (IES-R), fatigue (FSI), sleep (ISI), well-being (MHC-SF), resilience (CD-RISC 10), and quality of life (SF-20). The effects on conserved transcriptional response to adversity (CTRA) were examined by next-generation sequencing of dried whole blood samples.</div></div><div><h3>Results</h3><div>Twenty participants were enrolled with a mean age of 39.9 years (range 21–52 years). No significant changes were observed for the active stand test or 6MWT. A significant reduction in insomnia severity (ISI: 16.6 vs. 13.6; p = 0.001) was observed post-intervention, but scores reverted toward baseline levels at 4-week follow-up. No significant improvements were seen in autonomic symptoms, anxiety, perceived stress, depression, well-being, or COVID-19 related distress. Pro-inflammatory CTRA gene expression decreased significantly from pre-to post-intervention (<em>p</em> = 0.004). Declines in CTRA gene expression were most significant among those with 3 COVID-19 positive events (<em>p</em> = 0.01), followed by 2 events (p = 0.04) and 1 event (p = 0.05). Declines in CTRA gene expression did not vary significantly as a function of recent illness, COVID-19 hospitalization, demographic characteristics, or general medical history.</div></div><div><h3>Conclusion</h3><div>A virtual, six-week mindfulness program may improve sleep quality in women with Long COVID dysautonomia. While no objective improvement in dysautonomia symptoms were observed, our findings suggest a favorable effect of the mindfulness intervention on inflammatory and antiviral biology with a decrease in CTRA gene expression. Nonetheless, the symptom burden in this population is very high, and more attention is needed to provide effective multi-modal clinical therapies to this population.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100963"},"PeriodicalIF":3.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune-neuroendocrine crosstalk in mood and psychotic disorders: A meta-analysis and systematic review","authors":"Minne Van Den Noortgate ,&nbsp;Filip Van Den Eede ,&nbsp;Violette Coppens ,&nbsp;Erik J. Giltay ,&nbsp;Livia De Picker ,&nbsp;Manuel Morrens","doi":"10.1016/j.bbih.2025.100965","DOIUrl":"10.1016/j.bbih.2025.100965","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Bidirectional interactions between immune and neuroendocrine mechanisms are involved in mood and psychotic disorders, although individual studies report inconsistent and even contradictory findings on the nature of this crosstalk. Our objective was to perform an up to date systematic review and meta-analysis of the association between hypothalamic-pituitary-adrenal (HPA) axis and immune system functioning in mood and psychotic disorders.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We searched the Pubmed, Web of Science and Embase databases for studies reporting correlations between one or more HPA- and immune markers (IM) in patients with mood or psychotic disorders. We analyzed unchallenged correlations as well as challenge studies investigating the HPA-immune interaction through dexamethasone (DEX) and/or CRH suppression, HPA-mediated challenge of immune cell proliferation, immune challenges, or psychological stressors. Finally, genetic studies focusing on HPA x immune interrelation were evaluated. For meta-analyzable data, three primary outcome measures were defined for immune functioning, namely the pro-inflammatory index (PII) and anti-inflammatory index (AII) for the molecular IM and a composite cellular immune marker score (CCIM) for the cellular IM. Secondary analyses were performed for the individual molecular and cellular IM. Heterogeneity was evaluated with the I&lt;sup&gt;2&lt;/sup&gt; statistic. Meta-regression analyses were performed to evaluate the impact of potential covariates (publication year, gender, age, symptom severity) on the primary outcome analyses.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;93 studies (n = 8226) were included, of which 50 (n = 5649) contained meta-analyzable data. The majority of the included studies (k = 72) investigated major depressive disorder (MDD) patients, nineteen schizophrenia spectrum disorders (SSD) and six bipolar disorder (BD). Under physiological conditions, a poor association was found between cortisol and the PII only in the unmedicated subsample of MDD (k = 8; n = 425; r = .205; z = 2.151; p = .031) and the medicated subsample of SSD (k = 4; n = 152; r = .0.237; z = 2.314; p = .021). No significant correlation was found in MDD between the AII and cortisol (k = 3; n = 1243; r = .005; z = .188; p = .851). Similar results were found for the association between immune cell numbers and cortisol in both MDD (k = 10; n = 773; r = −.005; z = −.113; p = .894) and SSD (k = 4; n = 99; r = .167; z = 1.356; p = .175). A total of 42 studies discussed post-challenge associations between immune alterations and HPA disturbances, of which 12 (n = 389; all MDD) contained meta-analyzable data and 37 entered the systematic review (n = 1783). No post-DEX correlations were found between cortisol and PII (k = 3; n = 105; r = .074; z = .355; p = .722) or CCIM (k = 5; n = 259; r = −.153; z = −1.294; p = .196). However, a significant association was found between post-DEX cortisol/ACTH and PII produced by sti","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100965"},"PeriodicalIF":3.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How does chronic psychosocial distress induce pain? Focus on neuroinflammation and neuroplasticity changes","authors":"Barbara Fülöp ,&nbsp;Éva Borbély ,&nbsp;Zsuzsanna Helyes","doi":"10.1016/j.bbih.2025.100964","DOIUrl":"10.1016/j.bbih.2025.100964","url":null,"abstract":"<div><div>Chronic primary pain including fibromyalgia for the musculoskeletal system persists for more than 3 months. Its etiological factors and the pathophysiological mechanisms are not known, and therefore, there is no satisfactory therapy, it is an unmet medical need condition. The only etiological and aggravating factor is chronic psychosocial distress, which is known to cause neuroimmune and endocrine changes both in the periphery and the central nervous system. In this short review, we introduce our research perspective by summarizing the recent literature on the interactions between chronic pain, stress, and commonly co-morbid mood disorders. Immune activation, autoimmunity, neuro-immune-vascular crosstalks and neuroinflammation play roles in the pathophysiology of these conditions. Data on stress-induced neuroplasticity changes at cellular and molecular levels were also collected in relation to chronic primary pain both from clinical studies and animal experiments of translational relevance. Understanding these mechanisms could help to identify novel therapeutic targets for chronic primary pain including fibromyalgia.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100964"},"PeriodicalIF":3.7,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143403025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding, predicting, and treating depression in pregnancy to improve mothers' and offspring's mental health outcomes: The HappyMums study","authors":"A. Biaggi ,&nbsp;V. Zonca ,&nbsp;C. Anacker ,&nbsp;V. Begni ,&nbsp;F. Benedetti ,&nbsp;A. Bramante ,&nbsp;A. Braniecka ,&nbsp;V. Brenna ,&nbsp;M. Bulgheroni ,&nbsp;C. Buss ,&nbsp;L. Cavaliere ,&nbsp;C.A.M. Cecil ,&nbsp;A.C. Couch ,&nbsp;D. de Barra ,&nbsp;H. El Marroun ,&nbsp;S. Entringer ,&nbsp;R. Grassi-Oliveira ,&nbsp;M. Jackowska ,&nbsp;A. Korosi ,&nbsp;P.J.C. Kwant ,&nbsp;A. Cattaneo","doi":"10.1016/j.bbih.2025.100961","DOIUrl":"10.1016/j.bbih.2025.100961","url":null,"abstract":"<div><h3>Background</h3><div>Perinatal depression is common: on average, more than 13% of women suffer from physician-diagnosed disorder and 20% report symptoms bearing clinical relevance. Maternal depression not only significantly impacts women's quality of life but also increases the offspring's risk of negative developmental outcomes, including mental disorders, through a combination of maternal alterations in <em>in-utero</em> biology and postnatal rearing factors during the early period of life. The HappyMums project aims to improve our understanding of perinatal depression by identifying the factors that robustly predict risk and resilience in mothers and their offspring, determining underlying neurobiological mechanisms, and, finally, testing the efficacy of potential interventions.</div></div><div><h3>Methods</h3><div>HappyMums will use data from a large collection of cohorts and registries containing biological, clinical, socio-demographic, environmental, and lifestyle data. It will pool unique human samples of maternal blood, placenta, chorionic villi and amniotic fluid, analyzing these data alongside pre-clinical samples of brain, blood and placental tissue from models of prenatal stress in mice and livebearing fish for correlative analyses. HappyMums will develop a mobile application (App) to collect multiple data types from women for early screening and monitoring of depressive symptoms.</div></div><div><h3>Conclusion</h3><div>The findings generated by HappyMums will be clinically relevant as they will increase the knowledge on perinatal depression, with unprecedented benefits for the offspring and the society as a whole.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100961"},"PeriodicalIF":3.7,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}