Brain, Behavior, and Immunity最新文献

{"title":"Association of early life adversity and peer victimisation with psychopathology and inflammatory-metabolic risk in adolescents from the eBRAIN study: the role of sex and diet.","authors":"Xuemei Ma, Andrew J Lawrence, Pei Jung Chen, Rebecca Pollard, Svenja Kretzer, Nare Amasi-Hartoonian, Corentin Vallée, Lucas Andersen, Yifan Xu, Nur Najiah Zaidani Kamarunzaman, Naghmeh Nikkheslat, Craig Morgan, Seeromanie Harding, Carmine M Pariante, Mitul Mehta, Giovanni Montana, Sylvane Desrivieres, Chiara Nosarti, Ana Rodriguez-Mateos, Paola Dazzan","doi":"10.1016/j.bbi.2026.107080","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107080","url":null,"abstract":"<p><strong>Background: </strong>Adolescence is a sensitive developmental period during which psychosocial stress can become biologically embedded, increasing risk for psychopathology and inflammatory-metabolic dysregulation. Early life adversity (ELA, such as maltreatment and household dysfunction) and peer victimisation frequently co‑occur, yet their cumulative association with adolescent psychopathology and inflammatory-metabolic risk remains poorly understood. Diet may be a modifiable pathway linking stress to both psychopathology and inflammatory and metabolic processes, yet evidence integrating multiple adversities with both subjective and objective dietary measures is limited. This study aimed to investigate whether co-occurring ELA and peer victimisation were associated with adolescent psychopathology and inflammatory-metabolic markers, and to test whether diet mediated these associations.</p><p><strong>Methods: </strong>In an ethically and socio-economic diverse community sample of adolescents (N = 230, age: 12.9 ± 0.9 years), we assessed: 1) exposure to ELA and peer victimisation via structured interviews; 2) Internalising and externalising symptoms, using the Strengths and Difficulties Questionnaire (SDQ); 3) Age‑adjusted body mass index (BMI) and plasma levels of C‑reactive protein (CRP), as indicators of metabolic and inflammatory risk; and 4) Diet, using self‑reported dietary intake from a Food Frequency Questionnaire (FFQ) and urinary metabolic signatures of diet from spot urine samples measured via ultra-high-performance liquid chromatography and triple-quadrupole mass spectrometry (UHPLC-Q-q-Q MS). Linear regression models examined the associations between multiple exposures to ELA and peer victimisation with psychopathology, CRP and age-adjusted BMI, and mediation models tested the role of diet.</p><p><strong>Results: </strong>Participants exposed to both ELA and peer victimisation showed more internalising (B = 3.3, 95%CI: 2.0 to 4.6) and externalising symptoms (B = 3.9, 95%CI: 2.5 to 5.3), higher log<sub>10</sub>CRP (B = 0.4, 95%CI: 0.1 to 0.7) and age-adjusted BMI (B = 1.0, 95%CI: 0.3 to 1.6), and a higher likelihood of unhealthy dietary patterns (76% vs. 51%, pairwise p = 0.020), compared to those with no exposure. However, urinary metabolic signatures were not associated with adversity exposure. An unhealthy diet was associated with higher CRP (1.2 ± 3.8 vs. 0.4 ± 0.6 mg/L; p = 0.013), but not with psychopathology, and did not mediate associations between adversity and outcomes. Exploratory sex‑stratified analyses suggested that associations between multiple adversities and higher CRP and BMI were stronger in boys (log<sub>10</sub>CRP: B = 0.6, 95% CI: 0.2 to 1.1; age-adjusted BMI: B = 1.2, 95% CI: 0.2 to 2.2) than in girls (log<sub>10</sub>CRP: B = 0.2, 95% CI: -0.2 to 0.6; age-adjusted BMI: B = 0.6, 95% CI: -0.2 to 1.6), though the moderation effect for BMI did not reach statistical significance, but, again, diet did not m","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107080"},"PeriodicalIF":7.5,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Educational attainment and systemic inflammation: Evidence of a stable gradient from two measurements in the Tromsø study (2007-2016).","authors":"Julian Otero, Ilona Urbarova, Tom Wilsgaard, Hélène Colineaux, Therese Haugdahl Nøst, Raphaële Castagné, Christopher Sivert Nielsen, Lola Neufcourt, Sameline Grimsgaard, Dragana Vuckovic, Marc Chadeau-Hyam, Cyrille Delpierre, Michelle Kelly-Irving, Torkjel M Sandanger, Erlend Hoftun Farbu","doi":"10.1016/j.bbi.2026.107079","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107079","url":null,"abstract":"<p><p>Disadvantaged socioeconomic position (SEP) is associated with increased systemic inflammation. However, the mechanisms and potential persistence of these molecular differences remain poorly understood. We investigated the association between educational attainment, an indicator of SEP, and the levels of 52 plasma inflammatory proteins measured in the same individuals seven to eight years apart. We analyzed data from 909 participants of the sixth (2007-2008) and seventh (2015-2016) waves of the Tromsø Study, a longitudinal population-based study in Tromsø, Norway. Inflammatory protein levels were measured using the Olink Target 96 Inflammation panel and educational attainment was retrieved from questionnaires. Cross-sectional and longitudinal associations between educational attainment and inflammatory protein levels were assessed using multivariable linear models and linear mixed models, respectively. We identified a consistent association between higher educational attainment and lower levels of CCL20, CDCP1, and HGF, and higher levels of CST5 at both waves (FDR < 0.1). In addition, we observed that higher educational attainment was associated with lower levels of CCL19, IL-6, and OSM, and higher levels of FGF19 at the second wave only. Nonetheless, all associations were attenuated after adjustment for lifestyle factors, body-mass index, health conditions, and medication. Longitudinal analyses indicated a stable educational gradient across the two waves, with no significant changes in the association between educational attainment and inflammatory protein levels. Our findings indicate a stable educational gradient in the levels of several plasma proteins involved in cell migration, growth, and tissue remodeling in adults, across the seven-to-eight-year period, with modifiable lifestyle factors and body-mass index substantially attenuating the education-protein associations.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107079"},"PeriodicalIF":7.5,"publicationDate":"2026-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aerobic exercise ameliorates cardiac function in HFpEF mice by suppressing ALCAT1, neuroinflammation and oxidative stress in the paraventricular nucleus and nucleus tractus solitarius.","authors":"Yifang Zhao, Lili Zhang, Lili Feng, Yue Xi, Mengxin Cai, Zhenjun Tian","doi":"10.1016/j.bbi.2026.107078","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107078","url":null,"abstract":"<p><strong>Background: </strong>Heart failure with preserved ejection fraction (HFpEF) is commonly accompanied by sympathetic overactivation, contributing to poor patient prognosis. The paraventricular nucleus (PVN) and nucleus tractus solitarius (NTS) are critical cardiovascular regulatory centers. Pathological cardiolipin (CL) remodeling catalyzed by Acyl-CoA:lysocardiolipin acyltransferase 1 (ALCAT1) exacerbates disease progression. This study aims to elucidate the roles of aerobic exercise and ALCAT1 in modulating brain-heart axis dysregulation in HFpEF.</p><p><strong>Methods and results: </strong>We employed wild-type (WT) and Alcat1 knockout mice to establish an HFpEF model, followed by aerobic exercise. Neuroinflammatory model was established to investigate the role of ALCAT1 in neuroinflammation. Underlying mechanisms were explored in HT22 cells. In HFpEF mice, aerobic exercise suppressed ALCAT1 and up-regulated growth differentiation factor 5 (GDF5) in the PVN and NTS, reduced pro-inflammatory cytokines, enhanced antioxidant enzyme activities, decreased oxidative stress markers, and attenuated neuronal structural damage and hyperactivation. These central improvements were accompanied by attenuated cardiac sympathetic overactivation, lowered blood pressure, and improved diastolic function. The important role of ALCAT1 was further supported, as its genetic knockout conferred significant protection in both HFpEF and neuroinflammatory models. In HT22 cells, GDF5 suppressed the LPS-induced ALCAT1 up-regulation and ameliorated cellular injury.</p><p><strong>Conclusion: </strong>ALCAT1 is an important contributor to neuronal injury. Aerobic exercise suppresses ALCAT1 and up-regulates GDF5, ameliorating neuronal injury and improving diastolic function in HFpEF mice. Mechanistically, ALCAT1 and GDF5 are reciprocally regulated, which may contribute to the protective effects of aerobic exercise against HFpEF. These findings suggest ALCAT1 as a potential molecular target for exercise-based HFpEF therapy.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107078"},"PeriodicalIF":7.5,"publicationDate":"2026-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin ameliorates behavioral deficits in 5xFAD mice through modulation of neurogenesis, neuroimmune responses, neurotransmission, and metabolic pathways.","authors":"Jaydeep Roy, Ka Chun Tsui, Chi Him Poon, Jingyi Zhang, Yunfan Lai, Kan Yin Wong, Mazel Mihardja, Vera Tse, Pui Ching Li, Ching Au, Jonah Ng, Ersoy Kocabicak, Luca Aquili, Kah Hui Wong, Zhiliang Lu, Yasin Temel, Man Lung Fung, Lee Wei Lim","doi":"10.1016/j.bbi.2026.107077","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107077","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disorder with limited disease-modifying treatment options. Melatonin, an endogenous hormone, has been shown to have therapeutic effects on amyloid deposition, oxidative stress, and neuroinflammation in AD. However, the mechanisms of its neuroprotective effects in the hippocampus remain largely unknown. This study aimed to investigate the multi-mechanistic neuroprotective effects of melatonin in AD. Eight-month-old female 5xFAD transgenic mice were treated with melatonin (10 mg/kg) for 4 weeks. Temozolomide and bromodeoxyuridine were used to block neurogenesis and to label proliferating neurons, respectively. Our results showed that 5xFAD mice treated with melatonin exhibited improved exploratory behavior, enhanced memory performance, reduced depressive-like symptoms, and decreased levels of stress hormones. At the molecular level, melatonin reduced amyloid-beta (Aβ) plaque accumulation, elevated hippocampal neurogenesis markers (DCX and BrdU), increased Trem2 expression and anti-inflammatory microglial activation, restored serotonergic, dopaminergic, catecholaminergic, and GABAergic neurotransmission, and partially normalized broader hippocampal metabolic pathways. Notably, temozolomide treatment abrogated the beneficial effects of melatonin on memory performance and depressive-like behavior in 5xFAD mice, indicating a neurogenesis-dependent mechanism. Collectively, these findings suggest that melatonin ameliorates behavioral deficits in 5xFAD mice through both neurogenesis-independent (reduced Aβ plaque accumulation, Trem2-microglial activation, neurotransmission restoration, and metabolic remodeling) and hippocampal neurogenesis-dependent mechanisms. Overall, melatonin holds therapeutic potential for attenuating the neuropathology and behavioral deficits in AD.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107077"},"PeriodicalIF":7.5,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sedentary behavior as a Gut-Brain metabolic state.","authors":"Qian Yu, Zhihao Zhang, Zhenjun Tian, Jin Kuang, Karen D Corbin, Lauren E Oberlin, Audrey Collins, Bret H Goodpaster, Kirk I Erickson, Neville Owen, David W Dunstan, Charles H Hillman, Arthur Kramer, Teresa Liu-Ambrose, Cassandra Lowe, Matthew Heath, Hyo Youl Moon, William A Banks, Fred Paas, Natan Feter, David A Raichlen, Keith W Kelley, Jacob M Allen, Fabian Herold, Liye Zou","doi":"10.1016/j.bbi.2026.107068","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107068","url":null,"abstract":"<p><p>Sedentary behavior (SB) is prevalent in daily life, with a growing number of studies reporting that higher SB exposure is associated with poorer cardiometabolic and brain health. Thus, in line with a broader paradigm shift, SB should be considered as a postural and low-contractile metabolic state, shaped by both total exposure and bout patterning, that is related to, but distinct from, physical activity (PA), rather than simply the absence of the latter. Regarding the gut microbiome, current evidence on the role of SB remains limited and indirect, as human studies have not yet experimentally manipulated the SB exposure. To generate novel, yet testable hypotheses on the role of SB on the gut microbiome and brain health, this article synthesizes the current evidence base by emphasizing limitations related to cross-sectional designs, measurement heterogeneity, potential confounding by diet, sleep, medications, and PA, and the absence of established quantitative thresholds for SB exposure. Building on broader microbiome, metabolic, inflammatory, and gut-brain axis literature, we outline candidate pathways through which SB exposure, especially prolonged uninterrupted sitting, may alter microbe-derived metabolites and host responses, focusing on short-chain fatty acids, bile acid signaling, and tryptophan-derived metabolism alongside barrier-immune activation and autonomic-vagal circuitry relevant for brain health. Thus, this review extends prior SB-brain health frameworks by positioning SB as a specific gut-brain metabolic state with potential unique effects on a range of brain health-related outcomes. To probe the prediction that changes in SB patterns can affect gut-derived metabolites and specific brain health domains, suitable study designs are discussed. More specifically, future studies should combine accurate measures of SB and PA exposure with gut microbiome and blood-based metabolite assessments, vascular and inflammatory markers, autonomic measures, and standardized tests of cognition and mood, collected at different times, such as after meals and across the day, to better quantify and understand temporal dynamics. Approaching the gut-brain axis by isolating the effects of SB exposure is likely to generate practically relevant and impactful insights that not only help to inform stakeholders, such as policymakers, but also provide the basis for more fine-grained lifestyle recommendations to preserve and improve brain health.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107068"},"PeriodicalIF":7.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between markers of cellular ageing and of inflammation in bipolar disorders: Identification of IL-16 as an indicator of \"inflamm-ageing\".","authors":"Céline Bourdon, Luana Spano, Wahid Boukouaci, Ching-Lien Wu, Mohamed Lajnef, Ophélia Godin, Marion Leboyer, Bruno Aouizerate, Antoine Lefrere, Raoul Belzeaux, Philippe Courtet, Emilie Olie, Caroline Dubertret, Raymund Schwan, Paul Roux, Mircea Polosan, Ludovic Samalin, Vincent Hennion, Cynthia Marie-Claire, Bruno Etain","doi":"10.1016/j.bbi.2026.107061","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107061","url":null,"abstract":"<p><strong>Background: </strong>Bipolar disorder (BD) has been associated with biomarkers of ageing and of inflammation with little information about associations between markers.</p><p><strong>Method: </strong>Using blood samples of 139 individuals with BD, we generated Horvath, Hannum, EN, GrimAge and PhenoAge epigenetic ages and used a latent profile analysis to construct subgroups of individuals based on their profile of epigenetic age accelerations. In blood samples, we measured telomere length (TL), mitochondrial DNA copy number (mtDNAcn), and 29 markers of inflammation of which 18 were analyzed.</p><p><strong>Results: </strong>Univariate analyses showed higher levels of IL-16, IL-7, IL-10, IL-1RA, IL-12-IL-23p40, TNF-alpha, TNF-R1, ICAM-1, VCAM-1 and HLA-E in the epigenetically older group, and negative correlations between mtDNAcn and TNF-alpha, IP-10, VCAM-1 and IL-6R and one positive correlation between TL and IL-15. After Bonferroni correction, the associations between the epigenetically older group, IL-16 and HLA-E remained significant (p < 0.001). After adjustment for confounding variables, multivariate analyses confirmed an association between the epigenetically older group and higher levels of IL-16 (p = 0.001). Analyses of methylation of the IL-16 gene (26 sites) suggested that a lower methylation of cg20700699, located in an enhancer region, was associated with a higher level of IL-16 in the blood (p < 0.001).</p><p><strong>Conclusions: </strong>This study identified that an epigenetically older subgroup of individuals with BD were characterized by higher IL-16 blood levels. IL-16 may act as a central mediator linking immune activation, chronic inflammation, and accelerated biological ageing. If replicated, these results might support the concept of \"inflamm-ageing\" in BD.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107061"},"PeriodicalIF":7.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Feeling lonelier with reduced social contact in everyday life predicts elevated inflammation.","authors":"Rachel E Koffer, Stephanie J Wilson","doi":"10.1016/j.bbi.2026.107074","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107074","url":null,"abstract":"<p><p>Trait loneliness robustly predicts heightened inflammation and, in turn, poorer health. Nevertheless, the etiology of loneliness in daily life remains largely unexplored and is an important research direction. The current study examines a source of daily loneliness fluctuation: how daily loneliness increases with reduced social contact, i.e., loneliness reactivity. It further tests how loneliness reactivity relates to inflammation in the 2004-2009 Midlife in the United States study. Adults (N = 159, ages 35-83) completed 8 consecutive nightly telephone interviews in which they self-reported how lonely they felt and whether they spent less time with others than normal that day. Participants separately (M(SD)_{time_lag} = 1.75(15.52) months) provided blood samples assayed for interleukin (IL)-6, C-reactive protein (CRP), and tumor necrosis factor (TNF)-α. Loneliness reactivity slopes were extracted from multilevel models predicting daily loneliness from reduced social contact. Regression models tested associations between these slopes, a signature of reactivity, and inflammatory markers. Reduced social contact predicted higher daily loneliness [B(SE) = 0.20(0.03), p < 0.001], and individuals varied in this loneliness reactivity (Random SD: 0.34). In turn, higher loneliness reactivity predicted higher IL-6 [B(SE) = 0.79(0.39), p = 0.043], CRP [B(SE) = 1.47(0.66), p = 0.027], and TNF-α [B(SE) = 0.47(0.22), p = 0.035]. Findings highlight the importance of examining loneliness in daily life and reactivity as a novel dimension of daily loneliness. Results also suggest that future research should examine health implications of loneliness reactivity to reduced social contact in daily life for novel just-in-time interventions aiming to offset the health risks of loneliness.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107074"},"PeriodicalIF":7.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Birth by cesarean section remodels neonatal brain barriers and associated immune and metabolic pathways in mice.","authors":"Valentine Turpin, Jennifer Morael, Alexandre J C Cergneux, Hugo Blair, Elisa Cintado, Atreye Majumdar, Kaaviyaa Muthughavi, Baptiste Mateu, Carmen Tessier, Lorena Morales, Emily G Knox, Anna Ratsika, Katherine E Guzzetta, Ana Paula Ventura-Silva, Jennifer Shearer, Neil J Loftus, Emily G Armitage, Alan Barnes, Horst Schroten, Hiroshi Ishikawa, Gerard Clarke, Jonathan R Swann, John F Cryan, María R Aburto","doi":"10.1016/j.bbi.2026.107070","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107070","url":null,"abstract":"<p><p>Delivery mode shapes early-life physiology through multiple pathways, including stress and hormonal signalling, neonatal oxygenation, and exposure to maternal microbes. Cesarean section (CS) bypasses several of these processes and has been associated with altered immune maturation and neurodevelopmental outcomes in humans and animal models. Given that CS is known to disrupt gut barrier integrity and that gut and brain barriers operate as a coordinated network, we investigated whether CS affects early postnatal brain barriers. Using a mouse model, we compared CS-delivered pups to vaginally born (VB) controls at postnatal days 8-9. Brain barrier permeability and structure were assessed using tracer extravasation and vascular and tight junction analyses, choroid plexus immune populations were profiled, and metabolomics was performed in cortex and plasma. The blood-brain barrier in the medial prefrontal cortex was mostly preserved. In contrast, the blood-cerebrospinal fluid barrier (BCSFB) exhibited structural alterations in vascular and epithelial tight junction compartments. These changes were accompanied by immune remodelling, including expansion of antigen-presenting border-associated macrophages and reduced parenchymal microglia density. CS delivery increased brain tracer accumulation, consistent with altered barrier function during this developmental window. Metabolomic analyses revealed lower levels of key brain metabolites, including N-acetylaspartate, a marker of neuronal metabolic state. Together, these findings demonstrate that CS delivery induces early alterations in brain barrier function, BCSFB structure, the immune landscape, and metabolic profiles in mice. This identifies delivery mode as a key perinatal variable shaping neonatal brain physiology and establishes a framework for dissecting how birth context may influence long-term neurodevelopmental trajectories.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107070"},"PeriodicalIF":7.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parental exposure to severe, threatening stressors is associated with elevated inflammation in adolescent offspring independent of genetic reflatedness.","authors":"Lauren A Costello, Madeline Daugherty, Zach J Gray, Megan R Gunnar, George M Slavich, Brie M Reid","doi":"10.1016/j.bbi.2026.107076","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107076","url":null,"abstract":"<p><p>Although parental stressor exposure has been proposed as an intergenerational pathway linking adversity to offspring inflammatory risk, the relative contributions of biological versus postnatal environmental transmission remain unclear. To investigate, we examined whether parental exposure to severe, socially threatening stressors-life-threatening events, legal/criminal victimization, and bereavement-predicted inflammation in late adolescence, and whether this association (a) differed for internationally adopted versus non-adopted youth and (b) varied by the timing of parental stress exposure relative to the child's placement in the family. Participants were 193 adolescents (97 internationally adopted, 96 non-adopted; mean age = 15.69 years) and their parents. Parents' lifetime stressor exposure was assessed using the Stress and Adversity Inventory (STRAIN); fasting blood samples were obtained from youth to assess an inflammation composite (z-score sum of IL-6, TNF-α, and CRP) as the primary outcome, with individual marker analyses conducted to identify primary drivers of composite effects. In multivariable linear regression models adjusting for adolescent age, sex, time of blood draw, trunk tissue fat, and adoption status, greater parental life-threatening stressor severity was associated with higher adolescent inflammation composite scores (β = 0.085, SE = 0.038, p = 0.025; R² = 0.33), with IL-6 emerging as the primary driver of this effect (b = 0.034, SE = 0.014, p = 0.015; R² = 0.27), robust to adjustment for multiple comparisons (q = 0.044). This association did not differ by adoption status. Since the majority of parental life-threatening stressors occurred before the child entered the family, we examined timing in exploratory analyses; the association held when restricted to pre-placement stressor severity (β = 0.086, p = 0.027). These findings suggest that parents' exposure to severe, life-threatening stressors-particularly those preceding the child's entry into the family-is associated with greater inflammatory activity in adolescence. The comparable effects across adopted and non-adopted youth, combined with the pre-placement timing effect, are most consistent with postnatal environmental transmission mechanisms.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107076"},"PeriodicalIF":7.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shingles vaccination and dementia: Do the numbers add up?","authors":"Fergus Hamilton, George Davey Smith","doi":"10.1016/j.bbi.2026.107072","DOIUrl":"https://doi.org/10.1016/j.bbi.2026.107072","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"107072"},"PeriodicalIF":7.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}