Brain, Behavior, and Immunity最新文献

{"title":"Non-neuronal mechanisms in autism spectrum disorder (ASD): Microglia and astrocytes at the crossroads with neurons","authors":"Henna Jäntti ,&nbsp;Susanne Michels ,&nbsp;Enrico Cherubini ,&nbsp;Rashid Giniatullin ,&nbsp;Tarja Malm","doi":"10.1016/j.bbi.2026.106275","DOIUrl":"10.1016/j.bbi.2026.106275","url":null,"abstract":"<div><div>Autism spectrum disorder (ASD) is a group of complex neurodevelopmental conditions characterized by persistent deficits in social interaction, communication, and repetitive behavior. Although the etiology of ASD has traditionally been linked to neuronal dysfunctions, emerging evidence highlights the significance of non-neuronal cells, particularly microglia and astrocytes, in the pathophysiology of ASD. Although both glial cell types exhibit diverse functional states, microglia are primarily associated with eliminating unused neurons and synapses during early brain development, whereas astrocytes in the tripartite synapse mainly support synapse formation and actively regulate excitatory and inhibitory neurotransmission. Together, microglia and astrocytes complement each other in shaping a dynamic excitatory/inhibitory (E/I) network in the developing brain. Abnormal glial function during critical neurodevelopmental periods is emerging as a significant, and possibly even a leading factor in the E/I imbalance underlying ASD. In this review we highlight recent findings on how microglia and astrocytes contribute to E/I imbalance and other neuronal dysfunctions in ASD, particularly during the vulnerable prenatal period. GABAergic transmission, with a shift in the polarity of GABA action early in development, represents a particularly vulnerable target for aberrant modulation by glia. Recent transcriptomic and multi-omics studies show that signaling pathways thought to be neuron-specific can also be activated in glia at distinct developmental time points, shaping their unique contributions to ASD. This growing knowledge opens new perspectives for using glia-targeted therapeutic approaches for mitigating debilitating aspects of ASD.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106275"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984473","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":"Tumor–Macrophage–Nerve interactions drive neuroinflammation and neuropathic pain in prostate cancer perineural invasion","authors":"Shaaban A. Mousa ,&nbsp;Mohammed Shaqura ,&nbsp;Doaa Mohamed ,&nbsp;Xueqi Hong ,&nbsp;Susanne M. Krug ,&nbsp;Elsayed Y. Metwally ,&nbsp;Chalid Assaf ,&nbsp;Sascha Treskatsch ,&nbsp;Michael Schäfer","doi":"10.1016/j.bbi.2026.106280","DOIUrl":"10.1016/j.bbi.2026.106280","url":null,"abstract":"<div><h3>Objective</h3><div>Perineural invasion − a hallmark of cancers such as prostate and pancreatic − is strongly associated with severe, treatment-resistant pain. To dissect the neuron-specific mechanisms underlying this pain, we established a rat model of prostate cancer–associated perineural invasion to get insights into neuroinflammatory processes arising from direct tumor–nerve interactions and to provide a platform for evaluating targeted therapeutic strategies.</div></div><div><h3>Methods</h3><div>GFP-expressing AT-1 prostate cancer cells were directly microinjected into the perineurium of the sciatic nerve in syngeneic Copenhagen rats. Over 21 days, we assessed tumor progression, macrophage infiltration, and expression of pro-tumorigenic and pro-inflammatory mediators. Nociceptive behavior was monitored for mechanical, heat and cold stimuli. The MEK/ERK pathway was inhibited pharmacologically using the intrathecal phosphor-ERK1/2 inhibitor.</div></div><div><h3>Results</h3><div>Perineural AT-1 cell injection induced progressive tumor growth accompanied by increased polarized macrophage infiltration with a predominance of M1 macrophages and their associated pro-inflammatory cytokines (IL-1β, TNF-α). This response was further characterized by elevated levels of pro-tumorigenic (RANTES, IL-1ra, TIMP-1, VEGF, Ki67) along with upregulation of neuronal injury markers (ATF-3, NGF, and GDNF) in the sciatic nerve. In parallel, sustained upregulation of cAMP as well as phosphorylation of CREB and ERK1/2 was observed along pain pathways over a 21-dayperiod. Mechanical and heat hyperalgesia as well as cold allodynia progressively intensified over 21 days. Importantly, MEK/ERK inhibition with intrathecal PD98059 reversed perineural tumor-induced mechanical allodynia.</div></div><div><h3>Conclusion</h3><div>This model provides insight into neuroinflammatory tumor–macrophage–nerve interactions associated with neuronal hyperexcitability. Although focused in scope, it enables stepwise investigation of tumor-induced neuronal responses and offers a useful platform for evaluating neuroinflammatory mechanisms of tumor invasion and for identifying potential therapeutic targets.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106280"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973185","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":"Astrocytic FKBP5 regulates neuroinflammation and cognitive outcomes in male mouse models of excitotoxic epilepsy","authors":"Yu-Ling Gan ,&nbsp;Shang-Hsuan Lin ,&nbsp;Yu-Ping Kang ,&nbsp;Jia-Zhen Zhou ,&nbsp;Wei-Hsuan Huang ,&nbsp;Ping-Hua Sung ,&nbsp;Chia-Chi Hung ,&nbsp;Pei-Chien Hsu ,&nbsp;Shu-Yin Chu ,&nbsp;Feng-Shiun Shie ,&nbsp;I-Hui Lee ,&nbsp;Chung-Jiuan Jeng ,&nbsp;Yi-Hsuan Lee","doi":"10.1016/j.bbi.2026.106278","DOIUrl":"10.1016/j.bbi.2026.106278","url":null,"abstract":"<div><div>FK506-binding protein 51 (FKBP51, encoded by <em>FKBP5</em>) is a multisignaling cochaperone that regulates cellular stress responses and inflammatory signaling through the NF-κB pathway. Although FKBP51 is upregulated in reactive astrocytes, its role in epilepsy and excitotoxic neuroinflammation remains unknown. Excessive astrogliosis and impaired glutamate transporter-1 (GLT-1)-mediated glutamate clearance promote excitotoxicity and increase seizure susceptibility. Here, we investigated how both global and astrocyte-specific <em>Fkbp5</em> deletions influence seizure susceptibility, astrogliosis, neuroinflammation, and cognition in male mice subjected to a kainic acid (KA)-induced epilepsy mouse model. Global <em>Fkbp5</em> knockout (<em>Fkbp5</em>-KO) presented lower seizure activity along with decreased neuronal loss and astrogliosis in the hippocampus compared with the wild-type mice. Astrocyte-specific <em>Fkbp5</em> conditional knockout (a<em>Fkbp5</em>-cKO) mice similarly attenuated seizure severity, decreased astrogliosis, improved novel object recognition, and preserved GLT-1 expression in hippocampal CA3. Glia–neuron mixed cultures derived from <em>Fkbp5</em>-KO brains showed reduced NMDA-induced neurotoxicity and astrogliosis, accompanied by decreased NF-κB p65 phosphorylation. Notably, overexpression of an <em>Fkbp5</em> quadruple mutant that disrupts the FKBP51–NF-κB interaction inhibited proinflammatory lipopolysaccharide-induced astrogliosis and NF-κB activation. Transcriptomic analysis of <em>Fkbp5</em>-KO hippocampi further confirmed suppression of NF-κB-driven inflammatory pathways. In summary, astrocytic FKBP51 mediates reactive astrogliosis and GLT-1 downregulation, linking excitotoxic neuroinflammation with seizure susceptibility and cognitive impairment, and represents a potential intervention target for epilepsy.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106278"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984433","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":"One treatment does not fit all: Indications that spinning therapy benefits only a subgroup of patients with depression characterized by a T memory cell inflation profile","authors":"Sarah E. Fromme ,&nbsp;Gara Arteaga-Henríquez ,&nbsp;Bartholomeus C.M. Haarman ,&nbsp;Annemarie Wijkhuijs ,&nbsp;Raf Berghmans ,&nbsp;Trine Munk-Olsen ,&nbsp;Hemmo Drexhage ,&nbsp;Bernhard T. Baune","doi":"10.1016/j.bbi.2025.106228","DOIUrl":"10.1016/j.bbi.2025.106228","url":null,"abstract":"&lt;div&gt;&lt;div&gt;A proportion of patients diagnosed with major depressive disorder (MDD) exhibit signs of premature T cell aging, i.e. memory T cell inflation, characterized by elevated levels of memory CD4&lt;sup&gt;+&lt;/sup&gt; and CD8&lt;sup&gt;+&lt;/sup&gt; T cells. Physical endurance training, including spinning therapy (ST), is known to counteract both T cell aging and depression.&lt;/div&gt;&lt;div&gt;The primary aim of this randomized, treatment-as-usual (TAU)-controlled study was to investigate whether signs of T cell aging (determined prior to ST) characterized remitters and responders to the intervention.&lt;/div&gt;&lt;div&gt;Patients aged 18–65 years with a diagnosis of MDD (Hamilton Depression Rating Scale (HDRS) ≥ 13) were included and randomized 1:1 to TAU or TAU + ST. The intervention consisted of moderate-intensity cycling sessions (30 min, three times per week), for eight consecutive weeks. A total of 72 patients (n = 35 TAU, n = 37 TAU + ST) with complete baseline immunophenotyping were included in the analyses (49 % females; mean age, 32 years).&lt;/div&gt;&lt;div&gt;We found that remitters to TAU + ST displayed significantly higher baseline levels of CD8&lt;sup&gt;+&lt;/sup&gt; memory T cells, particularly T central memory (Tcm) cells and T effector memory cells re-expressing CD45RA (TEMRA) cells, compared to non-remitters. Correction for potential confounders and logistic regression analysis revealed that baseline levels of CD8&lt;sup&gt;+&lt;/sup&gt; Tcm cells showed the strongest predictive value in the TAU + ST group (OR = 7.66, &lt;em&gt;P&lt;/em&gt; = 0.03), suggesting that these cells may serve as treatment-specific predictors of remission to adjunctive ST. Post hoc stratification of patients based on the levels of CD8&lt;sup&gt;+&lt;/sup&gt;Tcm cells identified a subgroup of n = 20 patients exhibiting several signs of T cell inflation in both the CD8&lt;sup&gt;+&lt;/sup&gt; and CD4&lt;sup&gt;+&lt;/sup&gt; T memory cell populations. This subgroup was older and showed a higher prevalence of cytomegalovirus seropositivity, suggesting a state of post-infectious T cell senescence. In addition, this subgroup was characterized by higher remission rates to TAU + ST compared to TAU alone, particularly in the long run (i.e., 75 % vs. 42 % at week 8, and 75 % vs. 17 % at the end of the follow-up phase at week 24, &lt;em&gt;P&lt;/em&gt; = 0.03; note the small group sizes of n = 8 and n = 12 patients, respectively). Although no significant effects of add-on ST on CD8&lt;sup&gt;+&lt;/sup&gt; memory T cells were found, adjunctive ST significantly increased naïve CD4&lt;sup&gt;+&lt;/sup&gt; T cells and decreased effector memory CD4&lt;sup&gt;+&lt;/sup&gt; T cells within the senescent subgroup. Add-on ST was not superior to TAU in the entire group of patients with MDD.&lt;/div&gt;&lt;div&gt;Taken together, our findings suggest that patients with MDD with a T memory cell inflation profile may be the one and only who would benefit from TAU + ST as an add-on treatment strategy. These results support the development of personalized psychiatry approaches guided by immunological profiling and challenge the conventional “one-size-fit”","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106228"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800330","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":"Long-term NRF2-driven microglial repopulation mitigates microgliosis, neuronal loss and cognitive deficits in tauopathy","authors":"Lucía Viqueira ,&nbsp;Elisa Navarro ,&nbsp;Pilar Negredo ,&nbsp;Juan Antonio Bernal ,&nbsp;María Isabel Rodríguez-Franco ,&nbsp;Elena Tortosa ,&nbsp;Manuela G. López","doi":"10.1016/j.bbi.2026.106253","DOIUrl":"10.1016/j.bbi.2026.106253","url":null,"abstract":"<div><div>Tauopathies, including Alzheimer’s disease, feature chronic microglial reactivity that drives neuroinflammation and disease progression. Pharmacological microglial depletion and subsequent repopulation using colony-stimulating factor 1 receptor inhibitors have emerged as a potential therapeutic strategy to reprogram dysfunctional microglia. Despite promising short-term results, the long-term efficacy and pharmacological modulation of repopulated microglia remain poorly understood. Here, we investigated the long-term effects of microglial repopulation alone and in combination with the activation of the cytoprotective nuclear factor erythroid 2 p45–related factor 2 (NRF2) in an <em>in vivo</em> AAV-hTau^P301L induced model. Integrating different behavioural, immunohistological and transcriptomic analysis, we evaluated cognitive function, tau pathology, neuronal survival and glial reactivity. We found that, whereas microglial repopulation alone did not significantly affect disease progression, NRF2-driven microglial replenishment sustained cognitive function, prevented hippocampal neuronal loss and restored microglial phenotype. Transcriptomic analyses further revealed that the combined treatment modulated tau- associated mitochondrial gene expression changes. These results highlight the importance of shaping the fate of self-renewed microglia and propose NRF2-mediated microglial repopulation as a potential pharmacological strategy for the treatment of tauopathies.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106253"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145910649","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":"Neural oscillations serving abstract reasoning are differentially associated with inflammatory markers in people with HIV","authors":"Tony W. Wilson ,&nbsp;Mikki Schantell ,&nbsp;Sarah M. Dietz ,&nbsp;Samantha H. Penhale ,&nbsp;Kellen M. McDonald ,&nbsp;Kyla R. De Luca ,&nbsp;Molly E. Voller ,&nbsp;Lan D. Volberding ,&nbsp;Olivia R. Carusi ,&nbsp;Lucy K. Horne ,&nbsp;Yasra Arif ,&nbsp;Ryan Glesinger ,&nbsp;Jason A. John ,&nbsp;Hannah J. Okelberry ,&nbsp;Pamela E. May-Weeks ,&nbsp;Adam J. Case ,&nbsp;Matthew C. Zimmerman ,&nbsp;Rachel K. Spooner","doi":"10.1016/j.bbi.2025.106236","DOIUrl":"10.1016/j.bbi.2025.106236","url":null,"abstract":"<div><h3>Introduction</h3><div>Despite living a normal lifespan, people with HIV (PWH) are at a much greater risk of developing cognitive impairment. While the precise mechanisms are not fully understood, persistently high inflammation levels are thought to be a key contributor, as multiple studies have linked cognitive impairment and elevated inflammation. In contrast, evidence of a relationship between neural function and inflammatory activity is extremely limited in PWH and/or controls. Thus, in the current study, we integrate state-of-the-art dynamic functional brain mapping with measures of three inflammatory markers that have been widely reported as elevated in PWH.</div></div><div><h3>Methods</h3><div>A total of 142 participants (range: 20–66 years old; 64 PWH and 78 controls) completed a validated abstract reasoning task during magnetoencephalographic (MEG) imaging, underwent comprehensive neuropsychological testing, and provided a blood sample for plasma-based inflammatory marker analysis of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and interferon γ-induced protein 10 (IP-10). The two groups were matched on age, sex, race/ethnicity, body-mass index (BMI), handedness, anxiety, substance use, and common medical conditions such as diabetes. Oscillatory neural responses supporting abstract reasoning were imaged by applying a beamformer to the processed MEG data, and whole-brain, voxel-wise analyses were conducted using each individual’s CRP, TNF-α and IP-10 concentrations, controlling for age and BMI, to identify the differential impact of inflammation on oscillatory neural dynamics in PWH.</div></div><div><h3>Results</h3><div>PWH exhibited significantly higher levels on each of the three inflammatory markers and performed more poorly on the abstract reasoning task than matched controls, with CRP levels being significantly related to performance across all participants. Critically, TNF-α levels were significantly related to the strength of theta oscillations during abstract reasoning in the left inferior frontal gyrus, with higher TNF-α scaling with weaker theta and the strength of this relationship differing by group. A similar relationship among increasing CRP levels and decreasing gamma oscillations was found in the left inferior parietal cortices, while increasing CRP was also associated with decreasing gamma in the right dorsolateral prefrontal cortex across both groups, with the latter being coupled to behavioral performance in controls.</div></div><div><h3>Discussion</h3><div>These findings provide the first evidence linking elevated inflammatory levels to altered brain dynamics and performance in PWH. Such data provides crucial empirical evidence supporting the long-held view that elevated inflammation may be central to the higher rates of cognitive decline in PWH. Future work should examine whether decreasing these inflammatory levels leads to improvements in cognitive function in PWH.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106236"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145843641","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":"Corrigendum to “USP9X suppression attenuates NLRP3 inflammasome activation and ameliorates neuroinflammatory phenotypes with motor function recovery in murine models”. [Brain Behav. Immun. 132 (2026) 106215]","authors":"Yu Guo ,&nbsp;Xiaochuan Qi ,&nbsp;Ao Wang ,&nbsp;Tingting Zhan ,&nbsp;Kexin Duan ,&nbsp;Wenjie Ma ,&nbsp;Changqing Liu","doi":"10.1016/j.bbi.2026.106290","DOIUrl":"10.1016/j.bbi.2026.106290","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106290"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028417","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":"The COVID generation: the neurodevelopmental consequences of in-utero COVID-19 exposure","authors":"Susan Weiner ,&nbsp;Yao Wu ,&nbsp;Jacob Jenhao Cheng ,&nbsp;Melissa Liggett ,&nbsp;Cassianna McCants ,&nbsp;Esther Adegbulugbe ,&nbsp;Anna Mears ,&nbsp;Diedtra Henderson ,&nbsp;Nickie Andescavage ,&nbsp;Catherine Limperopoulos","doi":"10.1016/j.bbi.2025.106238","DOIUrl":"10.1016/j.bbi.2025.106238","url":null,"abstract":"<div><h3>Background</h3><div>In historical viral epidemics, such as the H1N1 influenza and Zika viruses, prenatal exposures were correlated with risk for neuropsychiatric conditions in offspring. However, the long-term effects of prenatal COVID-19 viral exposure on offspring neurodevelopment are still being discovered.</div></div><div><h3>Methods</h3><div>We prospectively recruited mother-baby dyads during the COVID-19 pandemic, who had been exposed to the SARS-CoV-2 virus during pregnancy (2020–2022) into a longitudinal infant brain development study and compared them to a low-risk normative pre-pandemic cohort (2016–2019). Quantitative 3-D volumetric magnetic resonance imaging (qMRI) was conducted at a neonatal visit when the infant was approximately 2 weeks of corrected age. Behavioral development was assessed using the Bayley Scales of Infant and Toddler Developmental, Third Edition (BSID-III) and the Infant-Toddler Social and Emotional Assessment (ITSEA), when the child was approximately 2 years old. An ordinary least squares regression model was used to determine the neurodevelopment of toddlers relative to their exposure to the SARS-CoV-2 virus. Mediation analyses were performed to assess how in utero exposure to SARS-CoV-2 affected the newborn brain and toddler developmental outcomes. Analyses were adjusted for maternal age and educational level, infant sex, and total brain volume on qMRI.</div></div><div><h3>Findings</h3><div>This study prospectively recruited 142 mother baby dyads, 103 from a normative prepandemic cohort and 39 pairs who had been exposed to the SARS-CoV-2 virus during pregnancy. In utero viral exposure was associated with altered newborn regional brain volumes in the cortical gray matter (<em>q</em> = 0.001), subcortical gray matter (<em>q</em> &lt; 0.001), cerebral white matter (<em>q</em> = 0.005), and left hippocampus (<em>q</em> = 0.008). Viral exposure additionally was associated with lower cognition (<em>q</em> = 0.010) and social emotional (<em>q</em> = 0.001) scores on the BSID-III and higher scores on the internalizing domain (<em>q</em> = 0.040) of the ITSEA. The lower cognition scores on the BSID-III following SARS-CoV-2 exposure were mediated in part by the altered cortical gray matter volumes (21.9 % mediated, <em>p</em> = 0.034). These lower cognition scores further mediated the relationship between the SARS-CoV-2 viral exposure and increased internalizing behavior scores on the ITSEA (61.0 % mediated, <em>p</em> = 0.040).</div></div><div><h3>Conclusions</h3><div>This study reports that in utero SARS-CoV-2 viral exposure was associated with decreased cognitive skills in toddlers at age 2, and this association was mediated by cortical gray matter volumes in the newborn brain. In addition, toddler cognitive scores further mediated an increase in toddler internalizing behaviors. These findings highlight the need for ongoing assessments for children born during the COVID-era.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106238"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145896493","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":"Stimulant use disorder indicative of increased serum soluble intercellular adhesion molecule-1 concentrations with altered brain reward and interoceptive processing","authors":"Kaiping Burrows ,&nbsp;Breanna A. McNaughton-Long ,&nbsp;Angela K. Yakshin ,&nbsp;Valerio Coussa ,&nbsp;Rayus Kuplicki ,&nbsp;Robin L. Aupperle ,&nbsp;Jonathan B. Savitz ,&nbsp;Martin P. Paulus ,&nbsp;Jennifer L. Stewart ,&nbsp;Leandra K. Figueroa-Hall","doi":"10.1016/j.bbi.2026.106261","DOIUrl":"10.1016/j.bbi.2026.106261","url":null,"abstract":"<div><div>Stimulant use disorders (STIM): (1) elicit compulsive behaviors that can lead to altered brain structure and function; and (2) trigger inflammatory responses by inducing the release of immune molecules, suggesting potential adverse effects. Our previous findings show that amphetamine use disorder is associated with altered neural processing during reward, interoception, and inhibitory control tasks. To extend these findings, we investigated links between neural processing and inflammation that may contribute to STIM. Participants from the first half of the Tulsa-1000 (T1000) study (<em>n</em> = 500) met criteria for either group: (1) stim+ (<em>n</em> = 49) reported methamphetamines/amphetamines as their current drug of choice and met criteria for past-year STIM; or (2) stim- (<em>n</em> = 90) endorsed no past-year diagnosis other than nicotine use disorder. Immunoassays were used to measure six inflammatory analytes. We examined blood oxygen-level-dependent (BOLD) responses to monetary incentive delay (MID), visceral interoceptive awareness (VIA), and inhibitory control with the stop signal task (SST) performed during functional magnetic resonance imaging. The stim+ group exhibited higher serum soluble intercellular adhesion molecule-1 (sICAM-1) concentrations than the stim- group, no significant differences or associations were found with the other inflammatory factors. Within the stim+ group, greater sICAM-1 levels were associated with: (1) lower right nucleus accumbens (NAc) BOLD signal during MID reward anticipation; and (2) higher right amygdala BOLD signal during interoceptive attention. No significant sICAM-1 associations emerged for the SST in stim+ . Inflammation may play a central role in stimulant use as indicated by increased sICAM-1, which may point to central mechanisms. The association between high inflammation and reduced NAc reward activation or higher interoceptive signals in STIM may reflect an STIM-sICAM-1 feedback loop mechanism.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106261"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917059","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":"Corrigendum to “The impact of repetitive neonatal procedural pain on cognitive behavioral development in male mice: A microglial perspective” [Brain Behav. Immun. 131 (2026) 106182]","authors":"Yueshu Wang ,&nbsp;Ru Ling ,&nbsp;Wen Zheng ,&nbsp;Dongqing Xia ,&nbsp;Cuiting Min ,&nbsp;Mengying Chen ,&nbsp;Wei Zhou ,&nbsp;Xiaonan Li","doi":"10.1016/j.bbi.2026.106288","DOIUrl":"10.1016/j.bbi.2026.106288","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106288"},"PeriodicalIF":7.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084244","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}