Journal of Neuroinflammation最新文献

{"title":"Modulation of neuronal α1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-κB/NLRP3 signaling pathway in Alzheimer's disease mice.","authors":"Bo Li, Li Wang, Yan Xiao, Zhi Tang, Yang Wang, Ting Sun, Xiaolan Qi","doi":"10.1186/s12974-025-03506-3","DOIUrl":"10.1186/s12974-025-03506-3","url":null,"abstract":"<p><strong>Background: </strong>Neuroinflammation is closely associated with the pathological progression of Alzheimer's disease (AD). The α1-adrenergic receptor (ADRA1), a G protein-coupled receptor, has been identified as a critical therapeutic target in inflammatory disorders. However, its precise mechanistic role in AD pathogenesis remains unclear.</p><p><strong>Methods: </strong>To investigate ADRA1's role in AD, we employed 3xTg-AD and wild-type (WT) mice, modulating neuronal ADRA1 expression via intracerebroventricular delivery of adeno-associated viruses. Cognitive function, tau pathology, neuronal morphology, and activation of the STING/NF-κB/NLRP3 signaling pathway were evaluated using behavioral tests, Western blot, Golgi-Cox staining, immunohistochemistry, and immunofluorescence. In vitro AD models were established using Aβ₄₂ oligomer-stimulated SH-SY5Y cells and primary murine neurons, along with SH-SY5Y cells transfected with full-length human tau (SH-SY5Y/htau). Pharmacological antagonists, inhibitors, lentiviral transduction, co-immunoprecipitation, and calcium flux assays were utilized to dissect ADRA1-mediated molecular mechanisms in tauopathy and neuroinflammation.</p><p><strong>Results: </strong>Hippocampal ADRA1 expression was significantly elevated in 10-month-old 3xTg-AD mice. Neuronal ADRA1 knockdown suppressed STING/NF-κB/NLRP3 pathway activation, ameliorated tauopathy and neuroinflammation, restored neuronal structure/function, and improved cognitive deficits in 3xTg-AD mice. Conversely, ADRA1 overexpression in C57/BL6 mice induced tauopathy, neuroinflammation, and cognitive impairment. Mechanistically, ADRA1 interacts with CXCR4 to form heterodimers, triggering cytoplasmic Ca²⁺ overload and subsequent STING/NF-κB/NLRP3 pathway activation.</p><p><strong>Conclusions: </strong>ADRA1 critically mediates tauopathy and neuroinflammation through STING/NF-κB/NLRP3 signaling. These results identify ADRA1 as a promising therapeutic target for AD prevention and treatment.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"187"},"PeriodicalIF":9.3,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers of progressive multiple sclerosis decrease following autologous hematopoietic stem cell transplantation.","authors":"Ida Erngren, Katarina Lundblad, Ivan Pavlovic, Asma Al-Grety, Anders Larsson, Kim Kultima, Joachim Burman","doi":"10.1186/s12974-025-03511-6","DOIUrl":"10.1186/s12974-025-03511-6","url":null,"abstract":"<p><strong>Background: </strong>Autologous hematopoietic stem cell transplantation (AHSCT) has been increasingly used for treatment of relapsing-remitting multiple sclerosis (RRMS). Existing data suggest that AHSCT might alter the natural course of multiple sclerosis (MS) and postpone or even prevent the occurrence of progressive MS. This study aimed to investigate whether three cerebrospinal fluid biomarkers of progressive MS: Galectin-9, GDF-15, and YKL-40, were affected by treatment intervention with AHSCT for RRMS.</p><p><strong>Methods: </strong>RRMS patients treated with AHSCT at Uppsala University Hospital between 2011 and 2018 were considered for participation and included if CSF samples from baseline and at least one follow-up were available. CSF from healthy volunteers was included as controls. Galectin-9 and GDF-15 concentrations were determined with ELISA, and YKL-40 with electrochemiluminescence.</p><p><strong>Results: </strong>The final cohort comprised 45 RRMS patients and 32 controls. At baseline, MS patients had markedly higher CSF concentrations of Galectin-9 and YKL-40 and slightly higher GDF-15 than controls. Following AHSCT, biomarker concentrations decreased from baseline to the 1-year follow-up, with a median (IQR) of 454 (357-553) vs. 408 (328-495) pg/mL (P = 0.0002) for Galectin-9; 49 (38-79) vs. 45 (35 to 75) pg/mL (P = 0.012) for GDF-15, and 100 (54-164) vs. 58 (43-92) ng/mL (P < 0.0001) for YKL-40. Galectin-9 and YKL-40 concentrations decreased further and were even lower at the 2-year follow-up; median (IQR) 408 (328-495) vs. 376 (289-478) pg/mL (P = 0.0009) for Galectin-9; and 62 (37-96) vs. 56 (30-83) ng/mL (P < 0.0001) for YKL-40. Thereafter, the levels of all biomarkers were stable throughout the follow-up.</p><p><strong>Conclusion: </strong>Treatment with AHSCT was associated with sustained reductions in biomarkers linked to progressive MS, indicating its potential not only to achieve lasting remission but also to delay or prevent transition to SPMS. However, additional studies are necessary to confirm these findings and elucidate their long-term clinical significance.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"186"},"PeriodicalIF":9.3,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rod-shaped microglia represent a morphologically distinct subpopulation of disease-associated microglia.","authors":"Yukio Matsuba, Kenichi Nagata, Yosuke Kadota, Naruhiko Sahara, Takaomi C Saido, Shoko Hashimoto","doi":"10.1186/s12974-025-03504-5","DOIUrl":"10.1186/s12974-025-03504-5","url":null,"abstract":"<p><p>Microglia, resident immune cells of the central nervous system, play an essential role in responding to pathological conditions by adopting diverse activation states and morphologies. Recent single-cell RNA sequencing have revealed that microglial subtypes were heterogeneous based on their gene expression profiles. However, the mechanism on how morphological changes in microglia are correlated with their gene expression profiles remains unclear. The current study aimed to identify a distinct population of rod-shaped microglia, characterized by an elongated morphology, in glutamyl cysteine ligase (GCLC)-deficient mice, a model of glutathione deficiency-induced oxidative stress. In the process of brain atrophy accompanied by neuronal cell death, which was observed in GCLC-KO mice, the rod-shaped microglia emerged in early stages of neurodegeneration and subsequently decreased in number over time. C1q-mediated synaptic pruning has been implicated in microglial activation under pathological conditions. Thus, whether C1q contributes to the formation of rod-shaped microglia was investigated. Notably, the genetic deletion of C1q did not affect the number or distribution of rod-shaped microglia in GCLC-KO mice. These findings suggest that their formation occurs via a C1q-independent mechanism. According to morphological and molecular analyses, the gene expression profile of the rod-shaped microglia was similar to that of the disease-associated microglia (DAM). To investigate the mechanisms underlying their formation, single-nucleus RNA sequencing was performed on cortical tissues collected from GCLC-KO mice. DAM-like microglial clusters were consistently identified. Further, pathway enrichment analysis suggested the potential involvement of the urokinase-type plasminogen activator (uPA, encoded by Plau) signaling. Considering the role of uPA in extracellular matrix degradation and cell migration, it may contribute to the morphological changes in rod-shaped microglia. In addition, the phosphorylation of growth-associated protein 43 (GAP43), a modification linked to structural plasticity, increased in rod-shaped microglia. Based on these findings, uPA signaling and phosphorylated GAP43 may be involved in microglial elongation and alignment along neuronal fibers, which potentially facilitate their migration during early neurodegenerative responses. Taken together, the rod-shaped microglia are a previously unrecognized activated population that emerges early in neurodegeneration and may be involved in disease-related processes. Understanding their molecular regulation can provide insights into early microglial responses and potential therapeutic targets.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"184"},"PeriodicalIF":9.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethanol consumption aggravates amyloid pathology and neuroinflammation in Alzheimer's disease associated with inflammasome activation and ASC speck propagation.","authors":"Veronika Brezani, Radhika S Joshi, Marti Ortega-Ribera, Prashanth Thevkar Nagesh, Viliam Brezani, Adam Zivny, Evelyn A Kurt-Jones, Douglas T Golenbock, Gyongyi Szabo","doi":"10.1186/s12974-025-03501-8","DOIUrl":"10.1186/s12974-025-03501-8","url":null,"abstract":"<p><strong>Background: </strong>Alcohol use disorder (AUD) has been associated with Alzheimer's disease (AD) and dementia, yet the underlying mechanisms and specific role of ethanol in AD progression remain poorly understood. Neuroinflammation has emerged as a key contributor to both AD pathogenesis and ethanol-induced brain damage. Activation of innate immune cells and signaling pathways, in particular NLRP3 inflammasome, plays a pivotal role in both AD and ethanol-induced inflammation. Thus, we postulated that excessive ethanol consumption could contribute to AD progression via amplified neuroinflammation.</p><p><strong>Methods: </strong>The 12-15-month-old WT and APP/PS1 mice received water or ethanol (3.5 g/kg) binge every alternate day for a period of one month. The effects of ethanol on amyloid pathology, microglia and astrocyte activation, and NLRP3 inflammasome activation were evaluated in the mouse brains. The effect of ethanol and amyloid β on NLRP3 inflammasome signaling was further studied in primary glial cells.</p><p><strong>Results: </strong>In this study, we show that repeated ethanol binges aggravate the amyloid pathology and plaque burden in the hippocampus of APP/PS1 mice. Furthermore, we demonstrate the additive effect of ethanol administration on NLRP3 inflammasome activation, IL-1β release, and ASC aggregation in the brains of APP/PS1 mice and primary glia cultures. Our study also reveals a strong astrocyte activation by ethanol in the hippocampus of APP/PS1 mice as demonstrated by significantly increased GFAP and ALDH1L1 protein levels. Further in vitro analysis revealed that ethanol potentiates the effect of amyloid β to increase the NLRP3 inflammasome activation in both primary astrocytes and microglia. Lastly, we demonstrate that glia-produced ASC specks induce IL-1β in microglia and astrocytes and induce ROS in SH-SY5Y neurons, contributing to sustained neuroinflammation in AD.</p><p><strong>Conclusion: </strong>Collectively, our results demonstrate that ethanol consumption exacerbates features of AD pathology associated with amplified neuroinflammation and NLRP3/ASC inflammasome activation, which may play an important role in the disease progression and severity.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"183"},"PeriodicalIF":9.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12265316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokine-complement cascade in glial-vascular units protects neurons from non-biogenic nanoparticles.","authors":"Ari Ogaki, Shinichi Kinoshita, Yuji Ikegaya, Ryuta Koyama","doi":"10.1186/s12974-025-03475-7","DOIUrl":"10.1186/s12974-025-03475-7","url":null,"abstract":"<p><p>Non-biogenic nanoparticles (NPs), including silica and polystyrene, are major components of environmental particulate pollution and can accumulate in the brain, especially during development when the blood-brain barrier is immature, leading to neurotoxicity. However, protective responses within the brain to these NPs remain poorly understood. Here, using a developing mouse model, we show that microglia phagocytose non-biogenic NPs through a complement-dependent mechanism involving C3 tagging. This process is regulated by a chemokine cascade in which vascular endothelial cells release CCL17, activating CCR4 on perivascular astrocytes to promote astrocytic C3 production. Inhibition of CCR4 signaling suppresses C3 production, impairs microglial phagocytosis, increases neuronal loss, and exacerbates anxiety-like behaviors. Our data establish a protective role for the vascular-glial chemokine-complement axis in limiting neurotoxicity during brain development. These findings reveal a coordinated immune response to non-biogenic environmental NPs and uncover a vascular-glial mechanism that mitigates NP-induced brain injury.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"182"},"PeriodicalIF":9.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12257687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular pathology of acute spinal cord injury in middle-aged mice.","authors":"Corey Fehlberg, Danny John, Brian Kang, James S Choi, Susana Cerqueira, Alexis Brake, Jae K Lee","doi":"10.1186/s12974-025-03494-4","DOIUrl":"10.1186/s12974-025-03494-4","url":null,"abstract":"<p><p>The median age at which spinal cord injuries occur has steadily increased from 29 to 43 over the last several decades. Although more pre-clinical studies in aged rodents are being done to address this shift in demographics, comprehensive transcriptomic studies investigating SCI pathobiology in middle-aged mice are lacking. To address this gap in knowledge, we compared behavioral, histopathological, and transcriptional outcomes in young (2-4 months old) and middle-aged (10-12 months old) mice. In contrast to most previous studies, open field tests showed no differences in locomotor recovery between the young and middle-aged mice over a one-month period. The injury site also demonstrated similar histopathology in terms of lesion size, and numbers of macrophages and fibroblasts. Acutely after injury, proliferation of macrophages, fibroblasts, and astrocytes were also similar between the two age groups. In addition, spatial transcriptomics showed similar, transcriptionally defined regions around the injury site at 3 days post-injury. However, single cell RNA-sequencing of the cells at the injury site and surrounding spared tissue showed differences in select cell subpopulations. Taken together, our results indicate that although young and middle-aged mice display similar locomotor recovery and histopathology after SCI, changes in cell subpopulations may underlie a decline in repair mechanisms that manifest after middle age.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"181"},"PeriodicalIF":9.3,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12257783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol in the CNS: functions, recycling and remyelination.","authors":"Emily C Wuerch, V Wee Yong","doi":"10.1186/s12974-025-03490-8","DOIUrl":"10.1186/s12974-025-03490-8","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"180"},"PeriodicalIF":9.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144618641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota-derived indoleacetic acid attenuates neuroinflammation and neurodegeneration in glaucoma through ahr/rage pathway.","authors":"Ning Wang, Chengyang Sun, Yijie Yang, Dandan Zhang, Lulu Huang, Chenrui Xu, Minghan Wang, Mengmeng Xu, Tongtong Yan, Yue Wu, Li Xu, Yahan Ju, Hao Sun, Wenyi Guo","doi":"10.1186/s12974-025-03505-4","DOIUrl":"10.1186/s12974-025-03505-4","url":null,"abstract":"<p><strong>Background: </strong>Gut microbiota has emerged as a promising therapeutic target for neurodegenerative disorders through regulation of neuroinflammatory responses, while its role in optic nerve degeneration remains incompletely characterized. This study elucidates the neuroprotective role of gut microbiota derived tryptophan metabolites in glaucoma through gut-eye communication and inhibition of microglia-mediated neuroinflammation.</p><p><strong>Methods: </strong>Gut microbiota profiling (16 S rRNA sequencing) and serum indoleacetic acid (IAA) quantification were performed in glaucoma patients versus controls. Microbiota-metabolite relationships were further validated through fecal microbiota transplantation (FMT). The neuroprotective and anti-neuroinflammatory effect of Bacteroides fragilis (B. fragilis) and IAA was assessed in both microbead-induced ocular hypertension mice model and in vitro BV-2 microglial cell inflammation model via immunofluorescence, qPCR, Western blot and mice behavioral assays. To explore the underlying mechanisms, retinal transcriptomics and microglia-neuron co-cultures were also employed.</p><p><strong>Result: </strong>Glaucoma patients exhibited gut dysbiosis characterized by depleted tryptophan-metabolizing bacteria (B. fragilis, Bacteroides thetaiotaomicron, Anaerostipes hadrus) and reduced serum IAA levels. Mice receiving FMT from glaucoma patients exhibited lower systemic IAA levels. In in vivo and in vitro models, B. fragilis or IAA restored AhR activation, suppressed inflammation by inhibiting microglial activation and the release of pro-inflammatory mediators throughout the retina, reduced retinal ganglion cells (RGCs) loss and preserved visual function. Mechanistically, IAA attenuated RAGE/NF-κB pathway activation via AhR-dependent signaling, conferring neuroprotection.</p><p><strong>Conclusion: </strong>Our study proposes a novel AhR-mediated gut microbiota-eye axis in glaucoma pathogenesis and demonstrates that IAA serves as an effective neuroprotective strategy with clinical potential for managing RGCs neurodegeneration.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"179"},"PeriodicalIF":9.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A systematic review of the causes and consequences of spreading depolarization in neuroinflammation; implications for neurovascular disorders.","authors":"Faheem Anwar, Olivia Grech, Caroline W Mugo, James A Roberts, Jessica C Hubbard, Chloe N Thomas, Alexandra J Sinclair, Lisa J Hill","doi":"10.1186/s12974-025-03503-6","DOIUrl":"10.1186/s12974-025-03503-6","url":null,"abstract":"<p><strong>Background: </strong>Spreading depolarization (SD) is a wave of neuronal and glial depolarization observed in various neurological conditions, including stroke, traumatic brain injury, subarachnoid haemorrhage, and migraine aura. This depolarization disrupts ion homeostasis, creating high energy demand for recovery. While healthy tissue can compensate, pathological tissue may develop ischemia, worsening brain injury and outcomes. Identifying inflammatory mediators that exacerbate neuroinflammation after SD could guide targeted therapies. This review aimed to explore both the neuroinflammatory effects of SD and the impact of experimentally induced inflammatory states on SD characteristics.</p><p><strong>Methods: </strong>PubMed and Scopus were systematically searched for preclinical studies that examined the effects of SD on inflammation, and the effects of an inflammatory state on SD responses. Data extracted included authors, publication details, study type, animal characteristics, group sizes, exclusions, relevant findings, and limitations. Additional details were collected for studies on SD and neuroinflammation, including induction methods, inflammatory markers and SD characteristics in altered inflammatory states.</p><p><strong>Results: </strong>Several studies indicated that SD triggered a robust neuroinflammatory response, marked by upregulation of cytokines-interleukin-1β, tumour necrosis factor-α, and interleukin-6-alongside transcription factors such as nuclear factor kappa B, and activation of astrocytes and microglia. Key mediators including toll-like receptors, cyclooxygenase-2 and high mobility group box 1 were also implicated, with evidence of neurogenic involvement via the release of calcitonin gene-related peptide. Differences in inflammatory responses were identified between single and multiple SD induction. Studies measuring the effect of altered inflammatory states on SD propagation were limited. Models of peripheral inflammation and non-demyelinating autoimmune encephalomyelitis did not lead to significant alterations in SD characteristics. However, administration of tumour necrosis factor was able to reduce SD amplitude, suggesting a possible neuroprotective effect.</p><p><strong>Conclusion: </strong>This review suggests potential mechanisms underlying the role of SD in neurological disorders. While SD is associated with inflammatory markers, evidence for the impact of heightened inflammatory states on cortical susceptibility to SD remains limited. Significant methodological variability and inflammatory disease models underscores the need for standardization to validate these findings. Further research into these mechanisms could identify novel therapeutic targets to mitigate SD-related neuroinflammation in neurological disorders.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"178"},"PeriodicalIF":9.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological inhibition of the cGAS-STING pathway suppresses microglia pyroptosis in sepsis-associated encephalopathy.","authors":"Qing-Quan Zeng, Yang Qi, Hui Yu, Ying Xu, Jin-Xing Chen, You-Wei Zheng, Gui-Fei Zhang, Qiao-Ling Zhang, Yan-Hua Zheng, Jing Guo, Zi-Hong Zhao, Fa-Sheng Wang, Gui-Lin Jin","doi":"10.1186/s12974-025-03507-2","DOIUrl":"10.1186/s12974-025-03507-2","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"176"},"PeriodicalIF":9.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}