Brain, Behavior, and Immunity最新文献

{"title":"Female mice exhibit similar long-term plasticity and microglial properties between the dorsal and ventral hippocampal poles","authors":"Eleonora De Felice ,&nbsp;Bianca Caroline Bobotis ,&nbsp;Giovanna Rigillo ,&nbsp;Mohammadparsa Khakpour ,&nbsp;Elisa Gonçalves de Andrade ,&nbsp;Cristina Benatti ,&nbsp;Antonietta Vilella ,&nbsp;Fabio Tascedda ,&nbsp;Cristina Limatola ,&nbsp;Marie-Ève Tremblay ,&nbsp;Silvia Alboni ,&nbsp;Laura Maggi","doi":"10.1016/j.bbi.2024.11.034","DOIUrl":"10.1016/j.bbi.2024.11.034","url":null,"abstract":"<div><div>The hippocampus is a heterogenous structure that exhibits functional segregation along its longitudinal axis. We recently showed that in male mice, microglia, the brain’s resident immune cells, differ between the dorsal (DH) and ventral (VH) hippocampus, impacting long-term potentiation (LTP) mainly through the CX3CL1-CX3CR1 signaling. Here, we assessed the specific features of the hippocampal poles in female mice, demonstrating a similar LTP amplitude in VH and DH in both control and <em>Cx3cr1</em> knock-out mice. In addition, the expression levels of <em>Cx3cr1</em> and <em>Cx3cl1</em> mRNA do not differ between the two poles in control mice. These data support the critical role of the CX3CL1-CX3CR1 signaling in setting the physiological amount of plasticity, equally between poles in females. Although BDNF is higher in DH compared to VH, the expression levels of inflammatory markers involved in plasticity and of phagocytosis markers in microglia are comparable between the two poles. In accordance, microglia soma and arborization area/perimeter, and microglial ultrastructure are similar across regions, with the exception of microglial density, cells arborization solidity and circularity that are higher in DH. Understanding the molecular processes underlying microglial sex differences and their potential implications for plasticity in specific brain regions is of major importance in physiological and pathological conditions.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 192-204"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766323","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":"Demyelination of the amygdala mediates psychological stress-induced emotional disorders partially contributed by activation of P2X7R/NLRP3 cascade","authors":"Yanning Li ,&nbsp;Yi Zhang ,&nbsp;Dandan Lin ,&nbsp;Xiaoliang Fu ,&nbsp;Chenchen Jing","doi":"10.1016/j.bbi.2024.12.023","DOIUrl":"10.1016/j.bbi.2024.12.023","url":null,"abstract":"<div><div>Psychological stress can lead to emotional disorders, such as anxiety and depression; however, the underlying mechanisms are complicated and remain unclear. In this study, we established a mouse psychological stress model using an improved communication box, in which the psychologically stressed mice received visual, auditory, and olfactory emotional stimuli from the mice receiving electric foot shock, thus avoiding physical stress interference. After the 14-day psychological stress paradigm, our mice exhibited a significant increase in depressive and anxious behaviors. We then performed proteomic liquid chromatography–tandem mass spectrometry for proteomic data analysis of the amygdala, and the results demonstrated that differentially expressed proteins were more enriched in myelin-related biological processes, cellular components, and molecular functions, indicating a correlation between psychological stress–induced emotional disorders and amygdala myelin damage. Molecular and morphological evidence further confirmed that psychological stress damages myelin ultrastructure, downregulated myelin basic protein and proteolipid protein expression, and reduced oligodendrocyte proliferation in the amygdala. Moreover, clemastine, an antimuscarinic and antihistaminic compound that has been shown to enhance oligodendrocyte differentiation and myelination, rescued depressive behaviors accompanied by increased oligodendrogenesis. In the amygdala, psychological stress was also noted to activate microglia and increase the levels of NOD-like receptor protein 3 (NLRP3) and the proinflammatory cytokines interleukin 1β and tumor necrosis factor α, as indicated by ELISA and Western blot analyses. Moreover, in stressed mice, the administration of Brilliant Blue G, a purinergic ligand-gated ion channel 7 receptor (P2X7R) antagonist, completely reversed the increases in NLRP3 and cleaved caspase-1 levels and partially prevented amygdala myelin damage. In conclusion, amygdala demyelination may mediate psychological stress–induced emotional disorders, and P2X7R/NLRP3 cascade activation partially contributes to amygdala myelin damage after psychological stress.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 365-375"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845686","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":"A Two-Year cohort study examining the impact of cytokines and chemokines on cognitive and psychiatric outcomes in Long-COVID-19 patients","authors":"Felipe Couto Amendola ,&nbsp;Guilherme Roncete ,&nbsp;Sophia Aguiar Monteiro Borges ,&nbsp;Cristiana Castanho de Almeida Rocca ,&nbsp;Antonio de Pádua Serafim ,&nbsp;Gabriela Salim de Castro ,&nbsp;Marilia Seelaender ,&nbsp;Euripedes Constantino Miguel ,&nbsp;Geraldo Busatto Filho ,&nbsp;Orestes V. Forlenza ,&nbsp;Rodolfo Furlan Damiano","doi":"10.1016/j.bbi.2024.12.006","DOIUrl":"10.1016/j.bbi.2024.12.006","url":null,"abstract":"<div><div>This study investigates the relationship between clinical, sociodemographic, and neuropsychological symptoms and serum cytokine concentrations with long-term cognitive and psychiatric outcomes in long-COVID-19 patients. We reassessed 108 adults who survived moderate to severe COVID-19 at two intervals post-discharge (T1, mean 6.9 months; T2, mean 23.5 months). Baseline sociodemographic and clinical data were collected from hospital records, while cognitive and mental health assessments included psychometric tests such as the Hospital Anxiety and Depression Scale (HADS) and Immediate and Delayed Recall Tests from the CERAD Battery. Serum cytokine levels were measured at T1. Generalized Additive Models (GAMs), Elastic Net Regression (NET), and Psychological Network Analysis (PNA) were used to analyze the data. The GAM analysis revealed significant associations between acute COVID-19 severity and Epworth Sleepiness Score with persistent anxiety symptoms at T2. For depression, both WHO severity class and Eotaxin levels were significant predictors. The Anti-inflammatory Index showed a marginally significant relationship with immediate recall, while age was marginally associated with delayed recall performance. In NET, only anxiety was significantly associated with Epworth Sleepiness Score, WHO severity class, and Proinflammatory Index. PNA did not reveal direct connections between cytokines and neuropsychological outcomes in the graphical model. However, centrality measures indicated that the Proinflammatory Index and VEGF were more central within the network, suggesting they might be important components of the overall system. This study provides insights into the complex role of cytokines and inflammation in long-COVID-19 outcomes, potentially aiding in the identification of biomarkers for diagnosis and prognosis.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 218-225"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817134","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":"Reevaluating feature importances in machine learning models for schizophrenia and bipolar disorder: The need for true associations","authors":"Yoshiyasu Takefuji","doi":"10.1016/j.bbi.2024.11.036","DOIUrl":"10.1016/j.bbi.2024.11.036","url":null,"abstract":"<div><div>Skorobogatov et al. developed supervised machine learning models to predict diagnoses and illness states in schizophrenia and bipolar disorder. However, their reliance on bootstrap forests and generalized regressions introduces significant biases in feature importance assessments. This paper highlights the critical distinction between feature importances generated by machine learning and actual associations, which are often model-specific and context-dependent. We underscore the limitations of biased feature importances and advocate for the use of robust statistical methods, such as Chi-squared tests and Spearman’s correlation, to reveal true associations. Reassessing findings with these methods will enable more accurate interpretations and reinforce the importance of understanding the limitations inherent in machine learning methodologies.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 123-124"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766338","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":"Neonatal exposure to morphine results in prolonged pain hypersensitivity during adolescence, driven by gut microbial dysbiosis and gut-brain axis-mediated inflammation.","authors":"Danielle Antoine, Junyi Tao, Salma Singh, Praveen Kumar Singh, Barbara G Marin, Sabita Roy","doi":"10.1016/j.bbi.2025.01.021","DOIUrl":"https://doi.org/10.1016/j.bbi.2025.01.021","url":null,"abstract":"<p><p>Opioids, such as morphine, are used in the Neonatal Intensive Care Unit (NICU) for pain relief in neonates. However, the available evidence concerning the benefits and harms of opioid therapy in neonates remains limited. While previous studies have reported that neonatal morphine exposure (NME) results in long-term heightened pain sensitivity, the underlying mechanisms are not well understood. This study proposes that dysbiosis of the gut microbiome contributes to pain hypersensitivity following NME. Using an adolescent female murine model, pain sensitivity was evaluated using tail flick and hot plate assays for thermal pain and the Von Frey assay for mechanical pain. Gut microbiome composition was assessed using 16 s rRNA sequencing, while transcriptomic changes in midbrain samples were investigated using bulk RNA-sequencing. NME induced prolonged hypersensitivity to thermal and mechanical pain in adolescence, accompanied by persistent gut microbial dysbiosis and sustained systemic inflammation, characterized by elevated circulating cytokine levels (e.g., IL-1α, IL-12p70, IFN-γ, IL-10). Transplantation of the microbiome from NME adolescents recapitulated pain hypersensitivity in naïve adolescent mice, while neonatal probiotic intervention with Bifidobacterium infantis (B. infantis) reversed the hypersensitivity by preventing gut dysbiosis and associated systemic inflammation. Furthermore, transcriptomic analysis of the midbrain tissues revealed that NME upregulated several genes and key signaling pathways, including those related to immune activation and excitatory signaling, which were notably mitigated by neonatal B. infantis administration. Together, these findings highlight the critical role of the gut-brain axis in modulating pain sensitivity and suggest that targeting the gut microbiome offers a promising therapeutic strategy for managing neurobiological disorders following early opioid exposure.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122211","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":"GDF15-GFRAL signaling drives weight loss and lipid metabolism in mouse model of amyotrophic lateral sclerosis","authors":"Germana Cocozza ,&nbsp;Ludovica Maria Busdraghi ,&nbsp;Giuseppina Chece ,&nbsp;Antonio Menini ,&nbsp;Marco Ceccanti ,&nbsp;Laura Libonati ,&nbsp;Chiara Cambieri ,&nbsp;Francesco Fiorentino ,&nbsp;Dante Rotili ,&nbsp;Ferdinando Scavizzi ,&nbsp;Marcello Raspa ,&nbsp;Eleonora Aronica ,&nbsp;Maurizio Inghilleri ,&nbsp;Stefano Garofalo ,&nbsp;Cristina Limatola","doi":"10.1016/j.bbi.2024.12.010","DOIUrl":"10.1016/j.bbi.2024.12.010","url":null,"abstract":"<div><div>Weight loss is a common early sign in amyotrophic lateral sclerosis (ALS) patients and negatively correlates with survival. In different cancers and metabolic disorders, high levels of serum growth differentiation factor 15 (GDF15) contribute to a decrease of food intake and body weight, acting through GDNF family receptor alpha-like (GFRAL). Here we report that GDF15 is highly expressed in the peripheral blood of ALS patients and in the hSOD1^G93A mouse model and that GFRAL is upregulated in the brainstem of hSOD1^G93A mice. We demonstrate that the localized GFRAL silencing by shRNA in the area postrema/nucleus tractus solitarius of hSOD1^G93A mice induces weight gain, reduces adipose tissue wasting, ameliorates the motor function and muscle atrophy and prolongs the survival time. We report that microglial cells could be involved in mediating these effects because their depletion with PLX5622 reduces brainstem GDF15 expression, weight loss and the expression of lipolytic genes in adipose tissue. Altogether these results reveal a key role of GDF15-GFRAL signaling in regulating weight loss and the alteration of and lipid metabolism in the early phases of ALS.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 280-293"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821789","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":"Preventive application of probiotics in ischemic stroke therapy through the gut-spleen-brain axis","authors":"Liqi Li","doi":"10.1016/j.bbi.2024.12.014","DOIUrl":"10.1016/j.bbi.2024.12.014","url":null,"abstract":"","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Page 294"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823742","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":"Ezrin-mediated astrocyte-synapse signaling regulates cognitive function via astrocyte morphological changes in fine processes in male mice","authors":"Lingmin Chen ,&nbsp;Jiao Jiao ,&nbsp;Fan Lei ,&nbsp;Bin Zhou ,&nbsp;Hong Li ,&nbsp;Ping Liao ,&nbsp;Xin Li ,&nbsp;Yi Kang ,&nbsp;Jin Liu ,&nbsp;Ruotian Jiang","doi":"10.1016/j.bbi.2024.11.022","DOIUrl":"10.1016/j.bbi.2024.11.022","url":null,"abstract":"<div><div>Astrocytes, which actively participate in cognitive processes, have a complex spongiform morphology, highlighted by extensive ramified fine processes that closely enwrap the pre- and post-synaptic compartments, forming tripartite synapses. However, the role of astrocyte morphology in cognitive processes remains incompletely understood and even controversial. The actin-binding protein Ezrin is highly expressed in astrocytes and is a key structural determinant of astrocyte morphology. Here, we found that Ezrin expression and astrocyte fine process volume in the hippocampus of male mice increased after learning but decreased after lipopolysaccharide injection and in a mouse model of postoperative cognitive dysfunction, both of which involved models with impaired cognitive function. Additionally, astrocytic Ezrin knock-out led to significantly decreased astrocytic fine process volumes, decreased astrocyte-neuron proximity, and induced anxiety-like behaviors and cognitive dysfunction. Astrocytic Ezrin deficiency in the hippocampus was achieved by using a microRNA silencing technique delivered by adeno-associated viruses. Down-regulation of Ezrin in hippocampal astrocytes led to disrupted astrocyte-synapse interactions and impaired synaptic functions, including synaptic transmission and synaptic plasticity, which could be rescued by exogenous administration of D-serine. Remarkably, decreased Ezrin expression and reduced astrocyte fine processes volumes were also observed in aged mice with decreased cognitive function. Moreover, overexpression of astrocytic Ezrin increased astrocyte fine process volumes and improved cognitive function in aged mice. Overall, our results indicate Ezrin-mediated astrocyte fine processes integrity shapes astrocyte-synapse signaling contributing to cognitive function.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 177-191"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695089","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":"Sick and detached: Does experimental inflammation impact on movement synchrony in humans?","authors":"Vera Flasbeck ,&nbsp;Fabian T. Ramseyer ,&nbsp;Manfred Schedlowski ,&nbsp;Harald Engler ,&nbsp;Martin Brüne","doi":"10.1016/j.bbi.2024.11.028","DOIUrl":"10.1016/j.bbi.2024.11.028","url":null,"abstract":"<div><div>Interpersonal connectedness is a central feature of human interaction that can be compromised during illness. Nonverbal signals play a crucial role in this context, and humans, like other animals, have evolved a behavioral immune system that enables individuals to detect subtle cues of sickness in others. Conversely, sick individuals often tend to avoid social interaction, a key component of sickness behavior. The coordination of body movements between two individuals (movement synchrony) is a measure of the quality of relationships that could provide insights into an interlocutor’s sickness state. In the present study, we explored the effect of lipopolysaccharide (LPS) administration, a naturalistic stimulus for inflammation-induced sickness, on movement synchrony in healthy volunteers randomly assigned to a double-blind interview with a non-treated interviewer conducted 2.5 h after intravenous injection of either LPS (N = 26) or placebo (N = 25). Movement synchrony was assessed by automated video analysis of subject’s and interviewer’s head movements. Lagged cross-correlations were used to objectively quantify coordination in dyads and to assess patterns of temporal movement synchronization. Data analysis revealed that dyads with subjects under placebo displayed a pattern of movement coordination comparable to that seen in previous studies. However, dyads with subjects under LPS showed a loss of simultaneous movement (i.e. moving at the same time) with the interview partner, which is normally the temporal domain providing the highest level of synchrony. Together, the findings suggest that immediate social interaction is attenuated when one interlocutor is exposed to systemic inflammation, while the other is unaffected. This effect can be attributed to both sickness behavior on one hand and correlates of the behavioral immune system on the other hand.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 157-162"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754699","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":"Plasma levels of matrix metalloproteinases in early psychosis, anxiety and depression: Evidence from the ALSPAC cohort","authors":"Lorenzo Ghelfi ,&nbsp;David Mongan ,&nbsp;Subash Raj Susai ,&nbsp;Melanie Föcking ,&nbsp;David R. Cotter ,&nbsp;Mary Cannon","doi":"10.1016/j.bbi.2024.11.035","DOIUrl":"10.1016/j.bbi.2024.11.035","url":null,"abstract":"<div><h3>Background</h3><div>Converging evidence supports the role of Matrix Metalloproteinases (MMPs) in psychiatric disorders. Originally identified as regulators of the extracellular matrix (ECM), MMPs’ functions span multiple processes, including inflammation, synaptic plasticity, neuronal migration, and blood–brain barrier maintenance. Tissue Inhibitors of Metalloproteinases (TIMPs) are major regulators of MMPs. In the present study we examined the associations of plasma MMPs and TIMPs with mental disorders in young adults aged 24 years in the Avon Longitudinal Study of Parents and Children (ALSPAC).</div></div><div><h3>Methods</h3><div>The present study was a nested case control study within the Avon Longitudinal Study of Parents and Children and comprised 374 participants who met criteria for psychiatric disorders (35 met the criteria for psychotic disorder, 201 for mild/moderate depressive disorder, and 266 for generalised anxiety disorder) and 401 controls. All cases and controls had were selected from the group of 4019 participants who had attended at age 24 years, completed psychiatric assessments and provided plasma samples. Plasma concentrations of MMP2, MMP3, MMP9 and TIMP-4 were quantified using proximity extension assays available on Olink® Cardiovascular Panel III. Logistic regression analysis compared standardised MMPs and TIMPs levels in cases and controls. Models were adjusted for sex, body mass index, and cigarette smoking.</div></div><div><h3>Results</h3><div>There was evidence for an association between MMP3 and depressive disorder (Odds ratio [OR] 1.35, 95 % confidence interval [CI] 1.06–1.73). There was evidence for an association between TIMP4 and depressive disorder (OR 1.51, 95 % CI 1.22–1.88) and generalised anxiety disorder (OR 1.43, 95 % CI 1.19–1.72). There was no evidence for an association between MMPs and psychotic disorders.</div></div><div><h3>Conclusions</h3><div>The study revealed that 24-year-olds with depressive and anxiety disorders exhibited elevated plasma concentrations of TIMP-4 compared to controls. There was evidence for an association between MMP3 and depressive disorder. These findings provide further support for the involvement of metalloproteinases as biomarkers in the pathophysiology of mental disorders during early adulthood.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"124 ","pages":"Pages 137-143"},"PeriodicalIF":8.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766329","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}