Brain, Behavior, and Immunity最新文献

{"title":"Higher CSF sTREM2 is related to slower hippocampal atrophy and cognitive decline independently of pTau181 levels","authors":"Henry Gilreath Stephenson ,&nbsp;Tobey J. Betthauser ,&nbsp;Erin Jonaitis ,&nbsp;Carol Van Hulle ,&nbsp;Gwendlyn Kollmorgen ,&nbsp;Clara Quijano-Rubio ,&nbsp;Michael Ewers ,&nbsp;Jannis Denecke ,&nbsp;Tyler K. Ulland ,&nbsp;Nathaniel A. Chin ,&nbsp;Ozioma C. Okonkwo ,&nbsp;Cynthia M. Carlsson ,&nbsp;Sanjay Asthana ,&nbsp;Sterling C. Johnson ,&nbsp;Kaj Blennow ,&nbsp;Henrik Zetterberg ,&nbsp;Barbara B. Bendlin","doi":"10.1016/j.bbi.2026.106468","DOIUrl":"10.1016/j.bbi.2026.106468","url":null,"abstract":"<div><div>Heightened <em>TREM2</em>-dependent microglial activation is thought to protect against the negative effects of Alzheimer’s disease (AD) neuropathology, but data in preclinical disease and in the context of aging are lacking. This study examined the association of longitudinal hippocampal atrophy and memory composite scores with baseline soluble TREM2 (sTREM2) in the cerebrospinal fluid in two large, well-characterized samples of elderly individuals. It was hypothesized that higher sTREM2 would be associated with slower atrophy and cognitive decline and that this effect would be stronger in those with higher AD neuropathology. Linear mixed effects models predicting hippocampal volume and cognitive decline tested interactions between sTREM2 and time (years since baseline) to see whether higher sTREM2 was associated with slower atrophy and cognitive decline, controlling for pTau181 and its interaction with time. A three-way interaction between pTau181, sTREM2, and time was then added to determine whether AD pathology moderated effects of sTREM2. Results showed that higher sTREM2 was associated with slower hippocampal atrophy and cognitive decline independently of pTau181 levels. Further analysis showed that cognitive effects were moderated by pTau181 levels such that beneficial effects of sTREM2 were stronger at higher levels of pTau181, though this effect was very small, and the interaction between sTREM2 and time remained significant. These findings suggest that higher <em>TREM2</em>-dependent microglial activation, as indexed by sTREM2, may indicate subtle resilience not just to the effects of AD but to age-related neurodegeneration more broadly.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106468"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146155621","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":"Dickkopf-1 release by the bone marrow upon ischemic stroke bridges neurovascular and immune deregulations","authors":"Romain Menet ,&nbsp;Maxime Bernard ,&nbsp;Sarah Lecordier ,&nbsp;Esther Trudel ,&nbsp;Anne-Sophie Allain ,&nbsp;Félix Distéfano-Gagné ,&nbsp;Josée Seigneur ,&nbsp;Natija Aldib ,&nbsp;Yacine Haili ,&nbsp;Frédéric Bretzner ,&nbsp;David Gosselin ,&nbsp;Ayman ElAli","doi":"10.1016/j.bbi.2026.106294","DOIUrl":"10.1016/j.bbi.2026.106294","url":null,"abstract":"<div><div>Neurovascular and immune alterations decisively govern definitive damage maturation after stroke. Dickkopf (DKK)1 elevated levels in the blood circulation of stroke patients correlate with poor outcomes. Herein, we report that <em>Dkk1</em> mRNA expression is not endogenously present in the healthy brain, and is barely and sparsely detectable at the lesion site in experimental ischemic stroke. Notably, we reveal a progressive increased protein expression of peripheral DKK1 in the subacute phase. Using genetic tools and bone marrow replacement approaches to mediate conditional DKK1 tissue-specific induction in conjunction with imaging, molecular, transcriptomic and functional studies, we demonstrate that DKK1 high levels at stroke onset accelerate subacute injury progression via deregulation of neurovascular functions. DKK1 prolonged post-stroke elevated levels mediate a chronic neuroinflammation associated with anxiety-like behaviors. DKK1 restricted induction in the bone marrow is sufficient to accelerate the subacute damage progression. DKK1 modulates the subacute peripheral immune response, suggesting that its <em>de novo</em> bone marrow expression represents a novel mechanism to regulate hematopoiesis in response to stroke. Neutralization of DKK1’s biological activity improves stroke outcomes. Our results indicate that DKK1 bone marrow release is a major determinant of definitive damage maturation after stroke and that its neutralization constitutes a promising disease-modifying therapeutic avenue.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106294"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017357","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":"BMP7 alleviates trigeminal neuralgia by suppressing oxidative stress and activation of satellite glial cells via the NRF2/HO-1 pathway","authors":"Meiqin Li ,&nbsp;Gaopeng Guan ,&nbsp;Xin Li ,&nbsp;Dingquan Zou ,&nbsp;Wei Zhang ,&nbsp;Kai Chen ,&nbsp;Yanying Xiao ,&nbsp;Yaping Wang ,&nbsp;Meng Wang","doi":"10.1016/j.bbi.2026.106277","DOIUrl":"10.1016/j.bbi.2026.106277","url":null,"abstract":"<div><h3>Background</h3><div>The trigeminal ganglion (TG) is a central hub for craniofacial injurious messaging, and its abnormal function is closely related to the pathogenesis of trigeminal neuralgia (TN). Bone morphogenetic protein 7 (BMP7), a pleiotropic cytokine with both neuroprotective and anti-inflammatory effects, has been shown to have therapeutic potential for neuropathic pain (NP) and neurodegenerative diseases. However, it remains to be elucidated whether BMP7 is involved in the pathological process of TN through the regulation of TG.</div></div><div><h3>Objective</h3><div>This study aimed to investigate whether BMP7 alleviates TN by modulating oxidative stress and activation in satellite glial cells (SGCs) of the TG.</div></div><div><h3>Methods</h3><div>A rat model of TN was established by chronic constriction injury of the distal infraorbital nerve (CCI-dION). Primary rat SGCs were activated with IL-1β to create an <em>in vitro</em> model. The role of BMP7 in regulating oxidative stress was assessed through <em>in vivo</em> knockdown and <em>in vitro</em> overexpression experiments. The NRF2 inhibitor ML385 was employed to validate the essential role of the NRF2/HO-1 pathway in BMP7-mediated SGC functional modulation.</div></div><div><h3>Results</h3><div>Following successful CCI-dION model establishment, TN rats showed significantly reduced mechanical pain thresholds, aggravated cold allodynia, and increased spontaneous pain behaviors, accompanied by decreased BMP7 expression, enhanced SGC activation, and elevated ROS levels in TG. These pathological phenotypes were consistently reproduced in BMP7-knockdown rats. In IL-1β-stimulated SGCs, BMP7 silencing mimicked pathological changes, while BMP7 overexpression reversed IL-1β effects − a rescue blocked by ML385. Critically, <em>in vivo</em> BMP7 overexpression attenuated CCI-dION-induced pain, oxidative stress, and SGC activation.</div></div><div><h3>Conclusion</h3><div>This study demonstrates that BMP7 alleviates TN by suppressing oxidative stress and activation of SGCs through activation of the NRF2/HO-1 pathway, highlighting its therapeutic potential for TN treatment.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106277"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984470","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":"Inhibition of the NFATc2/FKBP5 axis alleviates microglial neuroinflammation by regulating arachidonic acid metabolism in Parkinson’s disease","authors":"Yao Si ,&nbsp;Xue Zhao ,&nbsp;Lei Wu ,&nbsp;Xueying Li ,&nbsp;Pusheng Quan ,&nbsp;Shi Yan ,&nbsp;Xinyu Zhang ,&nbsp;Lige Han ,&nbsp;Lifen Yao ,&nbsp;Fan Yang","doi":"10.1016/j.bbi.2026.106296","DOIUrl":"10.1016/j.bbi.2026.106296","url":null,"abstract":"<div><div>Microglia-induced neuroinflammation is among the core pathological hallmarks of Parkinson’s disease (PD). FKBP5, which has been implicated in stress-related disorders, is recognized as a key regulator of inflammatory responses. However, the role and mechanism of FKBP5 in PD remain unclear. In the present study, we revealed that reducing FKBP5 levels via shRNA targeting microglia or pharmacological inhibition with SAFit2 could mitigate motor impairment and dopamine neuronal loss,<!--> <!-->as well as reduce<!--> <!-->arachidonic acid (AA) and proinflammatory factors (IL-6, TNF-α, and iNOS) levels in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Conversely, FKBP5 knockdown in 1-methyl-4-phenylpyridinium (MPP⁺)-treated BV2 microglia reduced inflammatory marker expression and targeted the inhibition of AA synthesis. Moreover, we revealed that NFATc2, a transcription factor of FKBP5, was significantly involved in AA generation and proinflammatory cytokine expression both <em>in vivo</em> and <em>in vitro</em>. In the MPP⁺-treated microglia, FKBP5 upregulation reversed the inhibition of AA signaling pathways induced by NFATc2 silencing. Furthermore, PD patients presented elevated mRNA expression of NFATc2 and FKBP5 in the peripheral blood, which were positively correlated with disease severity and serum AA levels, respectively. These findings highlight the involvement of the NFATc2/FKBP5 signaling pathway in AA-induced microglial neuroinflammation, indicating that NFATc2/FKBP5 may serve as PD biomarkers and targets for therapeutic interventions.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106296"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145996196","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":"Discovery of novel blood–brain barrier neuropathology in schizophrenia and bipolar disorder midbrain","authors":"Yunting Zhu ,&nbsp;Gerardo Mendez Victoriano ,&nbsp;Maree J Webster ,&nbsp;Frank A. Middleton ,&nbsp;Paul T. Massa ,&nbsp;Christine Fuller ,&nbsp;Cynthia Shannon Weickert","doi":"10.1016/j.bbi.2026.106292","DOIUrl":"10.1016/j.bbi.2026.106292","url":null,"abstract":"<div><div>Elevated pro-inflammatory cytokines and increased macrophage densities have been found in ∼ 35–50 % of schizophrenia and bipolar disorder brains. However, the influence of neuroinflammation on the blood–brain barrier (BBB) in these serious mental illnesses remains unclear. Here, we measured and compared multiple BBB-associated molecules in the ventral midbrain, including chemokines, macrophage markers, adhesion molecules, tight junction proteins, and basement membrane proteins in people with schizophrenia (n = 35), or bipolar disorder (n = 34), and controls (n = 33), stratified by inflammatory status. Both mRNA and protein levels of macrophage chemokine (CCL2) and macrophage scavenger receptor (CD163) were significantly elevated in the neuroinflammatory schizophrenia (high) compared to all the low inflammatory subgroups. Adhesion molecule mRNAs (ICAM1 and PECAM1) were increased in both schizophrenia and bipolar disorder high inflammatory subgroups, but PECAM1 protein was only elevated in schizophrenia, while ICAM1 protein was decreased in bipolar disorder. We found lower collagen IV (ColIV) protein levels in bipolar disorder. Tight junction protein claudin-5 (CLDN5) mRNA was elevated in both schizophrenia and bipolar disorder high inflammatory subgroups, while occludin (OCLN) mRNA was decreased in schizophrenia, especially in the high inflammatory subgroup. CLDN5 immunostaining revealed increased fragmented blood vessels with bursts of CLDN5 + processes surrounding and appearing to emanate from endothelial cells in schizophrenia and bipolar disorder high inflammation subgroup. Collectively, the high inflammatory individuals in both schizophrenia and/or bipolar disorder display more signs of BBB alterations, including increased macrophage chemoattraction, changed adhesion molecules, and altered tight junction proteins, though they have distinct molecular signatures of BBB pathology in the midbrain.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106292"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008993","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":"Prenatal-lactational alcohol exposure induces sex-specific CX3CL1/CX3CR1 dysregulation linked to neuroendocrine imbalance and cardiovascular risk","authors":"Dina Medina-Vera ,&nbsp;Alba García-Baos ,&nbsp;Mireia Medrano ,&nbsp;Laura Martín-Chaves ,&nbsp;Jorge Rodríguez-Capitán ,&nbsp;Fernando Rodríguez de Fonseca ,&nbsp;Antonia Serrano ,&nbsp;Manuel Jiménez-Navarro ,&nbsp;Olga Valverde ,&nbsp;Francisco Javier Pavón-Morón","doi":"10.1016/j.bbi.2026.106463","DOIUrl":"10.1016/j.bbi.2026.106463","url":null,"abstract":"<div><div>Fetal alcohol spectrum disorder is associated with lasting neurodevelopmental and cardiovascular dysfunctions. The fractalkine axis CX₃CL1/CX₃CR1, a chemokine and its sole known receptor expressed in microglia and myeloid/endothelial cells, coordinates neuroimmune and vascular responses. We tested whether prenatal-lactational alcohol exposure (PLAE) is associated with sex-specific dysregulation of this axis along with integrated behavioral, neuroendocrine, inflammatory, and cardiovascular signatures.</div><div>Pregnant C57BL/6 dams consumed 20% ethanol using a drinking-in-the-dark (DID) paradigm throughout gestation and lactation. Adult offspring (PND60–70) underwent behavioral testing (elevated plus maze and tail suspension test); plasma profiling of corticosterone, cytokines/chemokines, endothelial/coagulation markers, and matrix-remodeling enzymes; and cardiac transcriptional assays for stress- and inflammation-related genes (including <em>Cx3cr1</em>). Analyses were stratified by sex.</div><div>PLAE females exhibited increased anxiety-like behavior, two-fold higher plasma CX₃CL1, and upregulated cardiac <em>Cx3cr1</em> compared with control females. PLAE males showed no behavioral or endocrine changes but evidence of matrix remodeling (elevated proMMP-9, reduced sP-Selectin). Across sexes, PLAE was associated with a proinflammatory/endothelial-activation profile (elevated IL13, IL18, and PAI-1, reduced CXCL16, higher proMMP-9) and altered cardiac expression of <em>Nr3c2</em>, <em>Tnfrsf1a</em>, <em>Tlr4</em>, and <em>Nfkbia</em>, compatible with early vascular risk. Independent of exposure, females exhibited reduced immobility and higher corticosterone, IL5, IL13, sE-Selectin, and thrombomodulin. Plasma CX₃CL1 correlated inversely with exploratory and stress-coping behaviors, and positively with corticosterone, inflammatory/vascular markers, and cardiac <em>Cx3cr1</em> and <em>Tnfrsf1a</em>.</div><div>PLAE is associated with sex-specific dysregulation of the CX₃CL1/CX₃CR1 axis and convergent neuroimmune-vascular signatures indicative of subclinical endothelial dysfunction. These associative findings support the hypothesis that fractalkine-pathway modulation may mitigate long-term neurobehavioral and cardiovascular vulnerability after PLAE, warranting causal testing.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106463"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075710","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":"Wolf in sheep’s clothing: leveraging sheep to study how maternal immune activation contributes to neurodevelopmental disorders","authors":"Olivia C. Campbell,&nbsp;John R. Lukens","doi":"10.1016/j.bbi.2026.106474","DOIUrl":"10.1016/j.bbi.2026.106474","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106474"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075711","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":"Depression-related chronic stress promotes ovarian cancer progression via metabolic dysfunction and IRF1-mediated immune suppression","authors":"Yeqing Zheng ,&nbsp;Cheng Qian ,&nbsp;Shan Wu ,&nbsp;Bin Li ,&nbsp;Lin Zhang ,&nbsp;Wenjun Cheng","doi":"10.1016/j.bbi.2026.106471","DOIUrl":"10.1016/j.bbi.2026.106471","url":null,"abstract":"<div><div>Depression is highly prevalent among patients with ovarian cancer, but its impact on tumor progression and the underlying mechanisms remain unclear. This study aimed to investigate the relationship between depression and ovarian cancer progression, and evaluate the potential therapeutic value of antidepressant drugs. Clinical data analysis of patients with ovarian cancer revealed a significantly elevated risk of depression in this population. Animal experiments using chronic restraint stress (CRS) and chronic unpredictable mild stress (CUMS) models have confirmed that depression-related chronic stress induces depressive-like behaviors in mice and is associated with significant enhancement of ovarian cancer growth and metastasis. Mechanistically, single-cell RNA sequencing and metabolomics demonstrated that chronic stress downregulated interferon regulatory factor 1 (<em>IRF1</em>) expression in tumor cells. <em>IRF1</em> suppression inhibited the immune effector cells infiltration, such as macrophages, while inducing abnormal lipid metabolism and glutathione pathway dysfunction. Notably, combining antidepressant drugs with platinum-based chemotherapy reversed these pathological changes. This combination therapy upregulated <em>IRF1</em> expression, restored <em>CCR2⁺</em> macrophage infiltration, and delayed ovarian cancer progression in mice. Clinical validation further confirmed that high <em>IRF1</em> expression was correlated with prolonged overall survival (OS) in patients with ovarian cancer. These findings suggest that depression may be associated with ovarian cancer progression by remodeling the immune-metabolic microenvironment. This study highlights antidepressant therapy combined with anti-tumor treatment as a potential strategy for ovarian cancer patients with comorbid depression.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106471"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075665","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":"PPARγ in microglia helps protect adolescent male mice from harmful effects of stress during early development","authors":"Zhe Liu ,&nbsp;Jiutai Wang ,&nbsp;Yan Ge ,&nbsp;Yu Wang ,&nbsp;Hanyi Ling ,&nbsp;Yan Liu ,&nbsp;Jinqiang Zhang ,&nbsp;Zili You ,&nbsp;Yue Han","doi":"10.1016/j.bbi.2026.106483","DOIUrl":"10.1016/j.bbi.2026.106483","url":null,"abstract":"<div><div>Deficiency in the expression or activity of the nuclear hormone receptor peroxisome proliferator-activated receptor γ (PPARγ) has been observed in autism spectrum disorder, bipolar disorder and Alzheimer’s disease. Here we showed that separating mouse pups from their mothers for three hours daily during the first two weeks of life downregulated PPARγ, leading to pro-inflammatory polarization and activation of microglia in the hippocampus, which results in more severe responses to subsequent chronic restraint stress in adolescent animals. These effects of maternal separation were reversed by activating PPARγ with pioglitazone at 30 mg/kg/day for one week, which also stimulated hippocampal neurogenesis. Knocking out PPARγ specifically in microglia reduced neural activity and dendritic spine density in the cortex and hippocampus and led to depressive-like behaviors in mice. These results suggest that PPARγ expression enables microglia to “remember” previous exposure to stress and thereby influence responses to future stress. The findings may help guide interventions against stress and related psychological disorders.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106483"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164229","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":"Post-infection mental illness: Mapping pathways of vulnerability and resilience in VIRAL-MInds","authors":"Eva Wachtelaer ,&nbsp;Chloë Trippaers ,&nbsp;Ole A. Andreassen ,&nbsp;Ingrid Torp Johansen ,&nbsp;Nils Eiel Steen ,&nbsp;Helga Ask ,&nbsp;Dana Tzur Bitan ,&nbsp;Amit Kramer ,&nbsp;Sara Poletti ,&nbsp;Federica Colombo ,&nbsp;Livia De Picker","doi":"10.1016/j.bbi.2026.106291","DOIUrl":"10.1016/j.bbi.2026.106291","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"134 ","pages":"Article 106291"},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146002843","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}