Brain, Behavior, and Immunity最新文献

{"title":"Maltreatment exposure is associated with metabolomic disease risk scores in children.","authors":"Sonja Entringer, Malvika Godara, Ferdinand Hoffmann, Heiko Klawitter, Sibylle M Winter, Elisabeth B Binder, Claudia Buss, Christine Heim","doi":"10.1016/j.bbi.2025.106130","DOIUrl":"https://doi.org/10.1016/j.bbi.2025.106130","url":null,"abstract":"<p><p>Exposure to maltreatment during childhood is highly prevalent and a major risk factor for cardio-metabolic disorders that emerge in adult life, as well as for earlier mortality. Metabolite profiling technologies have emerged as a promising tool to detect biochemical aberrations occurring before the onset of symptoms or diseases to elucidate pathophysiology and aid risk prediction. Here, we tested the association in children between maltreatment exposure and metabolomics-based scores that predict cardio-metabolic diseases and mortality in later life. Maltreatment exposure was assessed using the using the Maternal Interview for the Classification of Maltreatment [MICM]. In N = 144 children exposed to maltreatment and a comparison group of N = 165 children without maltreatment experience (mean age = 8.04 years, range = 3.00-12.06), metabolomics assays were performed from fasting plasma samples, and risk scores (Diabetes, MetaboAge and MetaboHealth) for cardiovascular and metabolic diseases as well as mortality were computed. Maltreatment exposure was significantly and positively associated with all three scores after adjusting for sex and age. Metabolomics-based risk scores offer a promising avenue for guiding risk stratification and early precision interventions aimed at preventing or reversing biological risk trajectories associated with childhood maltreatment exposure before disease onset.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"106130"},"PeriodicalIF":7.6,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249892","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":"Expression of concern: \"Chemerin suppresses neuroinflammation and improves neurological recovery via CaMKK2/AMPK/Nrf2 pathway after germinal matrix hemorrhage in neonatal rats\" [BRAIN BEHAV IMMUN, Volume 70 (2018) 179-193].","authors":"Yixin Zhang, Ningbo Xu, Yan Ding, Yiting Zhang, Qian Li, Jerry Flores, Mina Haghighiabyaneh, Desislava Doycheva, Jiping Tang, John H Zhang","doi":"10.1016/j.bbi.2025.05.017","DOIUrl":"https://doi.org/10.1016/j.bbi.2025.05.017","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"101"},"PeriodicalIF":7.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022870","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":"Expression of concern: \"Recombinant Netrin-1 binding UNC5B receptor attenuates neuroinflammation and brain injury via PPARγ/NFκB signaling pathway after subarachnoid hemorrhage in rats\" [BRAIN BEHAV IMMUN, Volume 69 (2018) 190-202].","authors":"Zongyi Xie, Lei Huang, Budbazar Enkhjargal, Cesar Reis, Weifeng Wan, Jiping Tang, Yuan Cheng, John H Zhang","doi":"10.1016/j.bbi.2025.05.018","DOIUrl":"https://doi.org/10.1016/j.bbi.2025.05.018","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"129 ","pages":"100"},"PeriodicalIF":7.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022819","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":"Multimodal associations between brain morphology, immune-inflammatory markers, spatial transcriptomics, and behavioural symptoms in autism spectrum disorder.","authors":"Rosa Magaly Campêlo Borba de Morais, Flavia Venetucci Gouveia, Fabio Sato, Jürgen Germann, Sheila Pinheiro, Núbia Barros, Mayra A Kuroki, Camila Fongaro, Luiza Zaffarani, Marina Manzoni da Rocha, Rosana L Pagano, Erich T Fonoff, Helena P Brentani, Raquel C R Martinez","doi":"10.1016/j.bbi.2025.07.021","DOIUrl":"10.1016/j.bbi.2025.07.021","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Aggressive behaviour is a common and disruptive feature of autism spectrum disorder (ASD), affecting up to 68% of individuals and significantly burdening families and caregivers. Despite its prevalence, the mechanisms underlying aggression in ASD remain poorly understood, with evidence pointing to complex interactions between behavioural, neurobiological, and environmental factors. Emerging research suggests that neuroinflammation, along with structural brain changes, may contribute to aggressive behaviour in ASD.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objectives: &lt;/strong&gt;This study investigated the behavioural and neurobiological profiles of individuals with ASD who exhibit aggressive behaviour by examining neuroendocrine and inflammatory markers, structural brain differences, and spatial transcriptomics. The overarching goal was to identify the mechanisms underlying aggression in ASD and inform potential therapeutic strategies.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Forty-two male individuals with ASD aged 11-38 years were included in the study, divided into aggressive (Case; n = 21) and non-aggressive (Control; n = 21) groups based on Modified Overt Aggression Scale scores. A series of standardized questionnaires were used to investigate behaviour patterns and quality of life. Plasma levels of neuroendocrine and inflammatory markers, including cytokines and neuropeptides, were measured using a multiplex assay. For a subset of aggressive participants (n = 13), MRI scans were acquired, and deformation-based morphometry (DBM) was performed to evaluate structural brain differences. Spatial transcriptomics investigated gene expression patterns in brain regions exhibiting volume alterations.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Aggression in ASD was associated with more severe core symptoms (higher CARS scores) and pervasive behavioural disturbances, including hyperactivity, irritability, and stereotypy, as well as poorer quality of life. Aggressive individuals exhibited elevated levels of TNF-α, IL-6, IL-8, IL-13, IFN-γ, vasopressin, and epidermal growth factor (EGF), suggesting a pro-inflammatory state. Neuroimaging revealed distinct volume differences between patients with high- compared to medium-aggression, with enlargements in the anterior cingulate cortex, orbitofrontal cortex, and hippocampus and reductions in the amygdala, insula, and basal ganglia. Spatial transcriptomics identified two gene expression clusters: regions associated with emotional regulation exhibit overexpression of pro-inflammatory genes. In contrast, sensory and cognitive regions have relative anti-inflammatory gene upregulation, potentially reflective of a compensatory mechanism.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;This study identifies a complex interplay between heightened neuroinflammation and structural brain differences related to gene expression patterns in aggressive ASD. The findings suggest that aggression is associated with imbalances in the fronto-limbic-striatal ","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"1000-1013"},"PeriodicalIF":7.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144727998","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":"Blood-Brain barrier disruption in long COVID and cognitive correlates: A cross-sectional MRI study.","authors":"Leah H Rubin, Wen Shi, Alba Azola, Aparna Bhattacharyya, Raha M Dastgheyb, Jiani Wu, Christina Della Penna, Hannah Parker, Isabel Santiuste, Ana Ehrenspeck, Jennifer M Coughlin, Tracy D Vannorsdall, Hanzhang Lu, Rebecca Veenhuis","doi":"10.1016/j.bbi.2025.07.024","DOIUrl":"10.1016/j.bbi.2025.07.024","url":null,"abstract":"<p><p>Disruption of the blood-brain barrier (BBB) may contribute to neuropsychiatric symptoms observed in Long COVID (LC). Using a non-contrast magnetic resonance imaging (MRI) technique, we investigated BBB permeability in individuals with LC and its relationship to cognitive function. We hypothesized that LC individuals would show greater BBB permeability than recovered individuals, and that higher permeability would correlate with poorer cognition. Ninety-seven participants meeting the 2024 NASEM definition of LC with at least one neuropsychiatric symptom and 31 recovered controls completed an MRI scan and cognitive testing. BBB permeability was assessed using water-extraction-with-phase-contrast-arterial-spin-tagging (WEPCAST) MRI, which estimates the permeability-surface-area product (PS) of arterially labeled water entering the brain. Cognitive performance was summarized into eight factor scores derived from principal components analysis. Compared to controls, the LC group was older (M = 47 vs. 39 years, P = 0.003), less educated (P = 0.02), more likely female (P = 0.04), and had higher hospitalization rates for COVID-19 (P = 0.02). PS was significantly elevated in the LC group after adjusting for age and sex (B = 18.59, SE = 6.11, β = 0.28, P = 0.003). No significant group differences were found in cerebral blood flow, extraction fraction (E), or brain volume. Within the LC group, higher PS was associated with poorer motor function, but not with other cognitive domains. These findings indicate subtle but persistent BBB disruption in LC individuals over two years post-infection, with a potential link to motor dysfunction. This supports prior evidence of BBB changes following severe COVID-19 and suggests that BBB integrity may be a long-term biomarker of neuropsychiatric complications in LC.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"989-999"},"PeriodicalIF":7.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12409700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational diabetes mellitus induces 5-HT system dysfunction and exacerbates an ASD-like phenotype in male offspring by inhibiting the Ahi1/B9D1/Shh axis","authors":"Guangcheng Qin ,&nbsp;Hongbin Ni ,&nbsp;Wei Ren ,&nbsp;Zhuyun Wang ,&nbsp;Weiyan Yan ,&nbsp;Kemeng Li ,&nbsp;Xiaojing Lin ,&nbsp;Wei Zhang ,&nbsp;Xiaoyan Zhang ,&nbsp;Jiayu Li ,&nbsp;Yi Hou ,&nbsp;Min Wu ,&nbsp;Hua Zhang ,&nbsp;Lixue Chen ,&nbsp;Xiaoqiu Xiao","doi":"10.1016/j.bbi.2025.106127","DOIUrl":"10.1016/j.bbi.2025.106127","url":null,"abstract":"<div><div>Gestational diabetes mellitus (GDM) is a significant risk factor for autism spectrum disorder (ASD) in offspring. Despite the growing interest in the hypothesis of 5-hydroxytryptamine (5-HT) system dysfunction, the underlying mechanisms remain unclear and require further investigation. In this study, a GDM model was established in mice by feeding them a high fat diet (HFD) and administering an intraperitoneal injection of streptozocin (STZ). Our findings indicated that GDM exposure induced ASD-like behaviors and disrupted 5-HT system function by decreasing the level of Abelson helper integration site 1 (Ahi1) in the dorsal raphe nucleus (DRN) of male offspring. Furthermore, GDM evoked neuroinflammation, accompanied by a notable increase in the concentrations of proinflammatory factors (TNF-α, IL-1βand IL-6). Additionally, Ahi1 knockdown in normal mice mediated by an injection of AAV-Ahi1 in the brain recapitulated ASD-like behaviors and 5-HT system dysfunction, but these effects were blocked by the overexpression of B9 domain-containing protein 1 (B9D1) or meptazinol-mediated pharmacological activation of Ahi1, which ameliorated ASD-like behaviors, neuroinflammation and reversed 5-HT system dysfunction in male offspring of mothers with GDM (GDM-Os). Furthermore, lipopolysaccharide (LPS) induced neuroinflammation inhibited Ahi1 induced 5-HT system dysfunctions in vitro. Based on these findings, the inhibitory effects of meptazinol on GDM-induced ASD-like behaviors could be attributed to the involvement of 5-HT system dysfunction mediated by the Ahi1/B9D1/Shh axis. These findings provide novel insights into the mechanism by which neuroinflammation associated with GDM causes ASD pathogenesis and may pave the way for the development of a new therapeutic strategies for ASD.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"130 ","pages":"Article 106127"},"PeriodicalIF":7.6,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211633","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 broken barrier: neurovascular insights into long COVID","authors":"Chris Greene","doi":"10.1016/j.bbi.2025.106126","DOIUrl":"10.1016/j.bbi.2025.106126","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"130 ","pages":"Article 106126"},"PeriodicalIF":7.6,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205757","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":"Acid-sensing ion channel 3 in macrophages, but not sensory neurons, mediates development of activity-induced muscle pain.","authors":"Kazuhiro Hayashi, Joseph B Lesnak, Ashley N Plumb, Adam J Janowski, Lynn A Rasmussen, Heath Vignes, Robert Flanagan, Giovanni Berardi, William J Paradee, Kathleen A Sluka","doi":"10.1016/j.bbi.2025.106122","DOIUrl":"https://doi.org/10.1016/j.bbi.2025.106122","url":null,"abstract":"<p><p>Activity-induced pain is a significant symptom for people with chronic pain and reduces participation in daily activities and effective exercise programs. We previously showed that pharmacological blockade of ASIC3 locally in muscle, but not downregulation of ASIC3 in sensory neurons, prevents development of activity-induced muscle pain. Further, depleting macrophages from muscle prevents activity-induced pain. We therefore hypothesized that ASIC3 expression in muscle macrophages is necessary for development of activity-induced muscle pain by promoting release of pro-inflammatory cytokines. We developed a conditional ASIC3 knockout mouse (ASIC3^fl/fl) to test if removal of ASIC3 from macrophages prevents development of activity-induced pain. Cx3cr1^Cre+/ASIC3^fl/fl mice do not develop activity-induced pain; however, Adv^Cre+/ASIC3^fl/fl had no effect on activity-induced pain. In contrast, carrageenan-induced muscle pain was prevented in both Cx3cr1^Cre+/ASIC3^fl/fl and Adv^Cre+/ASIC3^fl/fl mice. Further, removal of ASIC3 from muscle macrophages, using a lentivirus expressing CRE injected into muscle from ASIC3^fl/fl mice, attenuated activity-induced pain. Flow cytometry revealed the proportion of muscle macrophages in muscle was decreased in Cx3cr1^Cre+/ASIC3^fl/fl compared to controls (Cx3cr1^Cre-/ASIC3^fl/fl), despite overall increases in myeloid cells and T-cells. Further in Cx3cr1^Cre+/ASIC3^fl/fl there was an attenuated release of the inflammatory cytokines GM-csf and TNFα from cultured macrophages treated with ATP and pH 6.5 when compared to controls. Together these data show that ASIC3 in muscle macrophages plays a critical role in development of activity-induced muscle pain by modulating release of inflammatory cytokines.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"106122"},"PeriodicalIF":7.6,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198308","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":"Targeting sex-specific DRG inflammation and neurofibrosis to prevent Bortezomib-induced neuropathy.","authors":"Michael B Thomsen, Abhishek Singh, Christina N Thebeau, Vivian D Gao, Nicholas F Schulze, Shannon M Landon, Oshri Avraham, Sarah X Yang, Shriya Koneru, Sami S Geier, Aidan Pelea, Valeria Cavalli, Stefanie Geisler","doi":"10.1016/j.bbi.2025.106124","DOIUrl":"10.1016/j.bbi.2025.106124","url":null,"abstract":"<p><p>Peripheral neuropathy is a common and often debilitating side effect of the chemotherapeutic agent bortezomib (BTZ), yet its mechanisms remain incompletely understood. To investigate the pathogenesis of BTZ-induced peripheral neuropathy (BIPN), we developed a mouse model that mimics the clinical route and prolonged duration of BTZ administration. In this model, male mice exhibited significantly greater sensorimotor deficits and axonal loss than females. Analysis of clinical data corroborated these findings, revealing that men with BIPN more frequently demonstrated absent sural nerve amplitudes and diminished distal sensation compared to women. To explore sex-specific responses to BTZ, we examined the dorsal root ganglia (DRG) microenvironment and found that BTZ primarily impacts non-neuronal cells. Among these, satellite glial cells (SGCs) exhibited the most pronounced baseline sex differences in gene expression and mounted the strongest transcriptional response to BTZ. In females with BIPN, SGCs upregulated genes involved in lipid metabolism, whereas in males, they strongly induced genes associated with extracellular matrix (ECM) remodeling, resulting in substantial collagen deposition in the DRGs. Because excessive ECM accumulation often reflects chronic immune activation, we investigated immune cell dynamics and observed a marked expansion of immune populations-particularly macrophages-in males. Depleting macrophages with anti-CSF1R in male mice attenuated BTZ-induced SGC reactivity, restored ECM homeostasis, preserved axons, and improved sensorimotor function. These findings implicate neuroinflammation and ECM dysregulation within the DRG as central mechanisms driving sex-specific vulnerability to BIPN and position the DRG microenvironment as a promising target for therapeutic intervention.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":"106124"},"PeriodicalIF":7.6,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198303","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":"Cannabidiol attenuates diet-induced metabolic endotoxemia, neuroinflammation, and anxiety-like behaviors in male aged rats","authors":"Jeferson Jantsch ,&nbsp;Fernanda da Silva Rodrigues ,&nbsp;Fernanda Wickert ,&nbsp;Gabriel de Farias Fraga ,&nbsp;Victor Silva Dias ,&nbsp;Yasmin Meireles Bitencourt ,&nbsp;Márcia Giovenardi ,&nbsp;Renata Padilha Guedes","doi":"10.1016/j.bbi.2025.106121","DOIUrl":"10.1016/j.bbi.2025.106121","url":null,"abstract":"<div><div>Obesity and aging synergistically reinforce neuroinflammation and disruption of homeostatic mechanisms, triggering pathological behaviors such as increased anxiety. Cannabidiol (CBD) has been reported to exert anxiolytic, anti-inflammatory, and neuroprotective effects, supporting the hypothesis that it may attenuate the detrimental consequences of obesity, even in aged animals. To test this hypothesis, 18-month-old male Wistar rats were divided into four experimental groups: control + vehicle (CT + vehicle), CT + CBD, cafeteria diet + vehicle (CAF + vehicle) and CAF + CBD. The animals were fed their diets for 8 weeks. Oral treatment with CBD (15 mg/kg/day) or vehicle began in the 9th week and continued until the end of the experiment, concurrently with the ongoing diet. We found that the CAF increased anxiety-like behaviors in the open field and elevated plus maze tests, while CBD mitigated these behaviors in the open field. Obesogenic diet also increased circulating levels of lipopolysaccharide, which were reduced by CBD. In the prefrontal cortex, CAF increased levels of interleukin 6 (IL-6), which were decreased by CBD. Additionally, CBD reduced the expression of tumor necrosis factor-α (TNF-α) and toll-like receptor 4 (TLR4). CAF feeding also caused a reduction in the main endocannabinoids, 2-arachidonoylglycerol (2-AG) and anandamide (AEA). In the prefrontal cortex, CAF increased transcripts of cannabinoid receptor 1 (CB1) and reduced those of cannabinoid receptor 2 (CB2) and serotonin receptor 5-hydroxytryptamine receptor 1A (HTR1A). Moreover, levels of triggering receptor expressed on myeloid cells 2 (TREM2) were reduced by the diet. These findings support the notion that obesity, through its metabolic and inflammatory consequences, exacerbates neuroinflammation and contributes to the dysregulation of the endocannabinoid system in aged animals. Notably, CBD demonstrated the ability to attenuate inflammatory markers and improve anxiety-like behavior, suggesting its potential as a therapeutic strategy to counteract obesity-induced neurobiological alterations in aging.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"130 ","pages":"Article 106121"},"PeriodicalIF":7.6,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191183","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}