Brain, behavior, & immunity - health最新文献

{"title":"Protocol for project MHISS: Mental Health and Immunodynamics of Social Stress","authors":"Daniel P. Moriarity ,&nbsp;Andrea C.M. Miller ,&nbsp;Japneet Kaur ,&nbsp;Ritika Prasad ,&nbsp;Matthew B. Figueroa ,&nbsp;George M. Slavich","doi":"10.1016/j.bbih.2025.100977","DOIUrl":"10.1016/j.bbih.2025.100977","url":null,"abstract":"<div><h3>Background</h3><div>Growing evidence suggests that immune alterations may mediate the impact of stress on a plethora of negative psychological and somatic health outcomes. In particular, social stress has been demonstrated to be a particularly potent type of stress that modulates immune activity. Typically, this effect has been tested in the lab with acute social stressors. To build upon this research with greater external validity, we used the transition to college campuses for 1st year undergraduates as an ecologically valid social stressor in this novel, intensive longitudinal psychoneuroimmunology study.</div></div><div><h3>Method</h3><div>This NIMH-funded study collected data from 173 incoming 1st year students at a large public university in California, USA. Eligible participants were recruited using an online screener disseminated by the University registrar's office and had to be 17–19 years old, fluent in English, living on campus, not have self-selected any roommates, and have moved at least 100 miles to campus. Enrolled participants completed a baseline survey, daily self-report measures (3589 reports total), and blood draws every three days for 22 days (656 assayed samples), as well as an additional survey on the 22nd day. The start of the daily surveys was timed so that students' 7th survey was their first full day on campus (i.e., the day after move-in). We also describe sub-studies involving (a) diagnostic interviews at the end of students' 1st academic year, (b) extending the daily surveys to capture a full month for participants with a menstrual cycle, and (c) piloting a college transition resilience program.</div></div><div><h3>Discussion</h3><div>Consistent with recent calls from the NIMH Director, this study uses the transition to college as an ecologically valid stress paradigm, in combination with novel intensive longitudinal assessment of immunology, to characterize social stress-related changes in biopsychosocial functioning over time. Studies resulting from this project will shed light on the dynamic interplay between key psychoneuroimmunological processes, advance the methodological standards of this field, and help identify intervention opportunities to improve mental health on college campuses and beyond.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100977"},"PeriodicalIF":3.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143724316","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":"Associations between the neural-hematopoietic-inflammatory axis and DNA methylation of stress-related genes in human leukocytes: Data from the Washington, D.C. cardiovascular health and needs assessment","authors":"Manuel A. Cintron ,&nbsp;Yvonne Baumer ,&nbsp;Alina P.S. Pang ,&nbsp;Elizabeth M. Aquino Peterson ,&nbsp;Lola R. Ortiz-Whittingham ,&nbsp;Joshua A. Jacobs ,&nbsp;Sonal Sharda ,&nbsp;Kameswari A. Potharaju ,&nbsp;Andrew S. Baez ,&nbsp;Cristhian A. Gutierrez-Huerta ,&nbsp;Erika N. Ortiz-Chaparro ,&nbsp;Billy S. Collins ,&nbsp;Valerie M. Mitchell ,&nbsp;Abhinav Saurabh ,&nbsp;Laurel G. Mendelsohn ,&nbsp;Neelam R. Redekar ,&nbsp;Subrata Paul ,&nbsp;Michael J. Corley ,&nbsp;Tiffany M. Powell-Wiley","doi":"10.1016/j.bbih.2025.100976","DOIUrl":"10.1016/j.bbih.2025.100976","url":null,"abstract":"<div><div>Chronic stress is associated with cardiovascular disease (CVD) risk and elevated amygdala activity. Previous research suggests a plausible connection between amygdala activity, hematopoietic tissue activity, and cardiovascular events; however, the underlying biological mechanisms linking these relationships are incompletely understood. Chronic stress is thought to modulate epigenomic modifications. Our investigation focused on associations between amygdala activity (left (L), right (R), maximum (M), and average (Av) AmygA), and splenic (SpleenA), and bone marrow activity (BMA) as determined by ¹⁸Fluorodeoxyglucose (FDG) on Positron Emission Tomography/Computed Tomography (PET/CT) scans. Subsequently, we assessed how these markers of chronic stress and hematopoietic activity might relate to the DNA methylation of stress-associated genes in a community-based cohort of African American individuals from Washington D.C. at risk for CVD. To assess the relationships between AmgyA, SpleenA, BMA, and DNA methylation, linear regression models were run and adjusted for body mass index and 10-year predicted atherosclerotic CVD risk. Among 60 participants (93.3% female, mean age 60.8), M-AmygA positively associated with SpleenA (β = 0.29; p = 0.001), but not BMA (β = 0.01; p = 0.89). M-AmygA (β = 0.37; p = 0.01 and β = 0.31; p = 0.02, respectively) and SpleenA (β = 0.73; p &lt; 0.01 and β = 0.59; p = 0.005, respectively) were associated with both IL-1β and TNFα. Decreased M-AmygA, SpleenA, IL-1β, and TNFα were associated with methylation of <em>NFκB1</em> at cg07955720 and <em>STAT3</em> at cg19438966. Our findings suggest a potential association between AmygA, SpleenA, and pro-inflammatory cytokines in the setting of chronic stress, suggesting an adverse hematopoietic effect. Furthermore, findings reveal associations with epigenetic markers of <em>NFκB</em> and <em>JAK/STAT</em> pathways linked to chronic stress.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100976"},"PeriodicalIF":3.7,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143643185","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":"Elevated TDP-43 serum levels associated with postoperative delirium following major cardiac surgery","authors":"Christopher Simon,&nbsp;Occam Kelly Graves,&nbsp;Oluwaseun Akeju,&nbsp;Tina B. McKay","doi":"10.1016/j.bbih.2025.100974","DOIUrl":"10.1016/j.bbih.2025.100974","url":null,"abstract":"<div><h3>Background</h3><div>Postoperative delirium is a recurring complication among vulnerable patients undergoing major cardiac surgery. While delirium has been associated with prodromal dementia, there is minimal evidence to support the causality of this nuanced relationship. Clarification as to how postoperative delirium might lead to neurodegenerative dementias, perhaps through evidence of contemporaneous biomarkers, would heighten the plausibility of a causal correlation. TAR DNA-binding protein 43 (TDP-43), a nuclear protein essential for transcriptional events, has been linked to pathological aggregation in Alzheimer's disease (AD) and AD-related dementias (ADRD).</div></div><div><h3>Methods</h3><div>Circulating TDP-43 levels in cardiac surgical patients aged 60 years and older were evaluated in a biobank derived from the Minimizing ICU Neurological Dysfunction with Dexmedetomidine-induced Sleep (MINDDS) clinical trial. Serum total TDP-43 levels, measured with a single molecule array (Simoa), were compared across preoperative and postoperative day one timepoints according to delirium status assessed using the Confusion Assessment Method (CAM). To investigate the temporal changes in serum TDP-43, an independent validation cohort of 25 patients aged 60 years and older undergoing major cardiac surgery was analyzed.</div></div><div><h3>Results</h3><div>Total serum TDP-43 levels increased by 16.5% (95% CI: 5.9%–27.9%, p = 0.0021) on postoperative day one compared to baseline levels. This increase was more pronounced in patients who experienced delirium (median increase of 55.1%, 95% CI: 22.9%–96.4%, p = 0.0002). Further, these findings were conserved in multiple logistic regression models adjusting for treatment, age, sex, and baseline cognitive scores. In the validation cohort, TDP-43 levels were found to be significantly elevated immediately following cardiopulmonary bypass from the baseline, with a gradual decrease by postoperative day one.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrate that post-cardiac surgery delirium among vulnerable patients is associated with significant elevations in circulating TDP-43. This relationship suggests that TDP-43 may serve as a prognostic biomarker for acute neurological insults and blood-brain barrier integrity following cardiac surgery. Overall, our results provide mechanistic insights into the inter-relationship between postoperative delirium and subsequent cognitive impairment, potentially offering new avenues for early intervention in at-risk surgical patients.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100974"},"PeriodicalIF":3.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143594157","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":"Observational and genetic evidence highlight the association of modifiable risk factors with the incidence and severity of neuroimmunological disorders","authors":"Jiang-wei Xia ,&nbsp;Jia-jian Li ,&nbsp;Yu Qian ,&nbsp;Jinmin Han ,&nbsp;Ming Lin ,&nbsp;Ming-yang Wang ,&nbsp;Teng Chen ,&nbsp;Guo-liang Chai ,&nbsp;Yi-nan Zhao ,&nbsp;Jun-wei Hao","doi":"10.1016/j.bbih.2025.100975","DOIUrl":"10.1016/j.bbih.2025.100975","url":null,"abstract":"<div><h3>Background</h3><div>Myasthenia gravis (MG), multiple sclerosis (MS), and neuromyelitis optica spectrum disorders (NMOSD) are a heterogeneous group of rare neuroimmunological disorders whose incidence rates have increased in recent years. The relationships between modifiable risk factors and neuroimmunological disorders are not fully understood.</div></div><div><h3>Methods</h3><div>We utilized multiple logistic regression to estimate the relationships between 38 modifiable risk factors and two neuroimmunological diseases using data from nearly 500,000 individuals in the UK Biobank. Additionally, we applied two-sample Mendelian Randomization (MR) analyses using genetic variants as instrumental variables to investigate the causal relationships of 32 modifiable lifestyle factors with 8 outcomes, representing risk and severity across three neuroimmunological diseases. To further explore the underlying mechanisms, mediation analysis was conducted to elucidate how significant associations might be mediated by intermediate variables.</div></div><div><h3>Results</h3><div>Our observational and MR analyses consistently found significant associations (P &lt; 0.05) indicating the number of cigarettes smoked daily, television watching, waist circumference, and BMI are all positively associated with the risk of developing MG. In contrast, moderate-to-vigorous physical activity and higher vitamin D levels are associated with a reduced risk of MS. Moreover, we discovered that the impact of television watching on the risk of MG was mediated by BMI (observational mediation analysis: 26.22%; MR mediation analysis: 9.90%).</div></div><div><h3>Conclusions</h3><div>These findings underscore the importance of modifiable risk factors in the development of neuroimmune diseases and support the identification of personalized intervention and prevention strategies. Notably, BMI significantly mediates the relationship between television watching and MG, indicating potential for targeted interventions to mitigate the risk of MG.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100975"},"PeriodicalIF":3.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143739451","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":"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}