Journal of neuroimmunology最新文献

{"title":"MOGAD optic neuritis after mild head/orbital trauma in six children","authors":"Alexander J. Sandweiss ,&nbsp;Jonathan Rosen ,&nbsp;Chaitanya Aduru ,&nbsp;Akansha Chandrasekar ,&nbsp;Kyla Blasingame ,&nbsp;Madhuri Chilakapati ,&nbsp;Rod Foroozan ,&nbsp;Jonathan M. Yarimi","doi":"10.1016/j.jneuroim.2025.578605","DOIUrl":"10.1016/j.jneuroim.2025.578605","url":null,"abstract":"<div><div>Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a potential cause of optic neuritis (ON). Its triggers and etiologies are not completely understood. We describe a novel clinical observation in six young patients with MOGAD-ON in the setting of strikingly parallel histories of mild head/orbital trauma. This is a single-center retrospective case series of six young patients and age-matched isolated MOGAD-ON controls. We present data both individually (de-identified, only the six trauma-associated cases) and in aggregate. Averages are presented as the arithmetic mean +/− SEM. 6/27 patients with MOGAD-ON, (3/6 female), between 8 and 18 years old presented with ON 5.5 days after mild head trauma. Four patients developed ON ipsilateral to their unilateral head trauma while two developed bilateral ON following midline head trauma. All patients tested positive for serum anti-MOG antibodies upon ON workup. They all received intravenous corticosteroids with rapid improvement in symptoms (5.5 weeks to full visual recovery) and none have since relapsed. No other patients with MOGAD-ON experienced preceding head trauma, and all patients in the control group were asked about trauma upon assessment of the history. Head trauma may serve as an inciting event in the presentation and diagnosis of MOGAD-ON. This novel observation provides a potential pathophysiologic mechanism independent of infectious triggers, although we cannot determine if these patients were already predisposed towards MOGAD-ON.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578605"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glial changes in the dentate gyrus of neuronal-specific PTEN knockout mice correlate with changes in cell proliferation","authors":"Sarah E. Latchney ,&nbsp;Anjali C. Raheja ,&nbsp;Brayan R. Ruiz Lopez ,&nbsp;Paige D. Womble ,&nbsp;Katherine J. Blandin ,&nbsp;Joaquin N. Lugo","doi":"10.1016/j.jneuroim.2025.578604","DOIUrl":"10.1016/j.jneuroim.2025.578604","url":null,"abstract":"<div><div>Dysregulated hippocampal neurogenesis is a feature of temporal lobe epilepsy (TLE), marked by increased neuronal proliferation. The tumor suppressor gene phosphatase and tensin homolog (PTEN) regulates neuronal proliferation, and its deletion is implicated in TLE. We have previously shown that deletion of neuronal subset-specific (NS)-PTEN in mice increases the number of proliferating cells throughout the dentate gyrus, including subregions that are typically devoid of neurons but rich in glial cells, most notably the Hilus and Molecular Layer. In this study, we hypothesized that NS-PTEN knockout mice would exhibit increased numbers of microglia and astrocytes in these same dentate gyrus subregions. We performed immunohistochemistry for Iba1 (microglia) and GFAP (reactive astrocytes) on wild-type and NS-PTEN knockout mice at 4 and 10 weeks of age. Our data reveal that NS-PTEN knockout mice exhibit increased Iba1+ cell density at both ages, with some male-specific effects. Subregional analysis of the dentate gyrus showed that at 4 weeks, NS-PTEN knockout mice had greater Iba1+ cell density in the Granule Cell Layer (GCL) and Hilus, and at 10 weeks, increases were observed in the GCL, Hilus, and Molecular Layer. Additionally, we observed an increased number of microglia with an amoeboid morphology and fewer with thin, ramified processes. Contrast to Iba1+ microglia, GFAP+ reactive astrocytes were localized to the neurogenic GCL. Importantly, increases in both glial types strongly correlated with heightened cell proliferation (Ki67+ cells), as reported in our previous study, underscoring the role of glial cells in the spatial dysregulation of neurogenesis in NS-PTEN knockout mice.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578604"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recurrent anti-NMDA receptor encephalitis in first-trimester pregnancy with initially antibody-negative CSF","authors":"Julia R. Jahansooz ,&nbsp;Alyssa M. Kameoka ,&nbsp;Jineane Shibuya ,&nbsp;Janette Abramowitz","doi":"10.1016/j.jneuroim.2025.578602","DOIUrl":"10.1016/j.jneuroim.2025.578602","url":null,"abstract":"<div><div>Anti-<em>N</em>-methyl-<span>d</span>-aspartate receptor (anti-NMDAR) encephalitis is a paraneoplastic autoimmune encephalomyelitis that predominantly affects females in their reproductive years <span><span>Dalmau et al., 2007</span></span> and <span><span>Dalmau et al., 2019</span></span>. It has been infrequently reported during pregnancy <span><span>Dono et al., 2023</span></span> and <span><span>Joubert et al., 2020</span></span>. We describe a case of a 25-year-old G4P2 patient at 11 weeks gestation with a history of anti-NMDAR encephalitis who presented with intermittent confusion for two weeks. Initial antibody tests for anti-NMDAR encephalitis in the cerebrospinal fluid (CSF) were negative. Repeat serum labs drawn upon readmission to the emergency department (ED) 3 weeks later were positive, and results were confirmed with repeat CSF testing. Following treatment, the patient returned to baseline and delivered a developmentally healthy, full-term baby. Current gold-standard testing for anti-NMDAR encephalitis is through detection of NMDAR antibodies in the CSF <span><span>Gresa-Arribas et al., 2014</span></span>. However, CSF antibody testing early in the disease course may not be as sensitive as traditionally thought, and repeat testing is indicated if high suspicion continues.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578602"},"PeriodicalIF":2.9,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baicalin-Geniposide combination modulates microglia polarization against chronic cerebral ischemia and concomitant kidney injury via the HIF-1α/EPO/NF-κB pathway","authors":"Tian Hu ,&nbsp;Qianqian Sun ,&nbsp;Jiahao Zhang ,&nbsp;Xuewei Zhou ,&nbsp;Jie Gong ,&nbsp;Yuan Li ,&nbsp;Chuan Wang ,&nbsp;Jiping Liu ,&nbsp;Bin Wang","doi":"10.1016/j.jneuroim.2025.578601","DOIUrl":"10.1016/j.jneuroim.2025.578601","url":null,"abstract":"<div><h3>Background</h3><div>Baicalin and geniposide combination (BC/GD), a traditional Chinese medicine pairing, is beneficial for chronic cerebral ischemia (CCI) and kidney injury, but the underlying mechanism remains unknown.</div></div><div><h3>Methods</h3><div>Using network pharmacology, we identified targets and pathways of BC/GD in CCI and kidney injury. Using molecular docking, we discovered the affinity between BC/GD and the key targets HIF-1α, EPOR, and TNF-α. Then, these were verified in SD rats and transwell co-cultures of HMC3 and HK-2 cells.</div></div><div><h3>Results</h3><div>Experimental validation demonstrated that BC/GD ameliorated cerebral and kidney pathological injury, cognitive impairment, and kidney dysfunction, increased cerebral blood flow, inhibited microglia activation and polarization of pro-inflammatory phenotypes, increased the expression of HIF-1α and EPOR, and reduced the phosphorylation of NF-κB and the level of pro-inflammatory factors in CCI rats. Then, in vitro validation experiments, we found that 12.5 μM and 25 μM BC/GD significantly increased the levels of anti-inflammatory factors and modulated the HIF-1α/EPO/NF-κB pathway in oxygen-glucose-deprived HMC3 and HK-2 cells, which was partially antagonized by PX-478, an inhibitor of HIF-1α.</div></div><div><h3>Conclusion</h3><div>BC/GD alleviated cerebral and kidney inflammatory injury, and its mechanism may be related to the modulation of microglia polarization through HIF-1α/EPO/NF-κB.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578601"},"PeriodicalIF":2.9,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143746183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interleukin-1 beta and Interleukin-6 serum concentrations correlate with neuropathy and liver enzyme levels in patients diagnosed with alcohol use disorder","authors":"Michail Papantoniou ,&nbsp;Stylianos Chatzipanagiotou ,&nbsp;Panagiotis Kokotis ,&nbsp;Chrysoula Nikolaou ,&nbsp;Antonios Gargalionis ,&nbsp;Elias Tzavellas ,&nbsp;Thomas Paparrigopoulos ,&nbsp;Michail Rentzos","doi":"10.1016/j.jneuroim.2025.578599","DOIUrl":"10.1016/j.jneuroim.2025.578599","url":null,"abstract":"<div><div>Peripheral neuropathy is a common clinical manifestation in patients diagnosed with alcohol use disorder (AUD). The pathogenesis of alcohol-related neuropathy is under investigation and there are insufficient data to support the hypothesis of a possible immune-mediated pathway. In this study, we correlated serum cytokine concentrations with neurophysiological and biochemical findings and investigated possible risk factors, pathogenetic mechanisms and biomarkers of neuropathy in patients with AUD. Ninety patients with AUD (54 with neuropathy and 36 without neuropathy) and sixty-eight age- and gender-matched healthy subjects (control group) were recruited in this prospective study over a period of three years. Serum concentrations of Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-10, and Tumor Necrosis Factor-alpha (TNF-α), as well as fasting glucose, blood thiamine and liver enzymes levels, were determined upon admission. The mean values of the concentrations of IL-1β, IL-6, IL-8 and TNF-α of patients with AUD were significantly higher than those of the healthy control group. We also found that the mean values of IL-1β and IL-6 concentrations were significantly higher in the group of patients with neuropathy than the patients without polyneuropathy and the healthy control group. Moreover, we found a statistically significant association between higher IL-1β, as well higher IL-6, concentration values and higher liver enzyme levels. Our study suggests that higher concentrations of circulating IL-1β and IL-6 may contribute in the pathophysiology of alcohol-related peripheral neuropathy, and that their concentrations are associated to time- and dose-dependent liver dysfunction.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578599"},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143738408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential roles for microglia in drug addiction: Adolescent neurodevelopment and beyond","authors":"Maricela X. Martinez,&nbsp;Stephen V. Mahler","doi":"10.1016/j.jneuroim.2025.578600","DOIUrl":"10.1016/j.jneuroim.2025.578600","url":null,"abstract":"<div><div>Adolescence is a sensitive period for development of addiction-relevant brain circuits, and it is also when people typically start experimenting with drugs. Unfortunately, such substance use may cause lasting impacts on the brain, and might increase vulnerability to later-life addictions. Microglia are the brain's immune cells, but their roles in shaping neural connectivity and synaptic plasticity, especially in developmental sensitive periods like adolescence, may also contribute to addiction-related phenomena. Here, we overview how drugs of abuse impact microglia, and propose that they may play poorly-understood, but important roles in addiction vulnerability and progression.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"404 ","pages":"Article 578600"},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143792192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of Baicalin against experimental obsessive compulsive disorder: Evidence from CSF, blood plasma, and brain analysis","authors":"Abhinay Dhiman ,&nbsp;Divya Choudhary ,&nbsp;Sidharth Mehan ,&nbsp;Pankaj Kumar Maurya ,&nbsp;Arun Kumar Sharma ,&nbsp;Aakash Kumar ,&nbsp;Ritam Mukherjee ,&nbsp;Sumedha Gupta ,&nbsp;Zuber Khan ,&nbsp;Ghanshyam Das Gupta ,&nbsp;Acharan S. Narula","doi":"10.1016/j.jneuroim.2025.578598","DOIUrl":"10.1016/j.jneuroim.2025.578598","url":null,"abstract":"<div><div>Obsessive-Compulsive Disorder (OCD) is a complex neuropsychiatric condition characterized by recurrent obsessions and compulsions, significantly impacting an individual's functionality and quality of life. This study aimed to explore the neuroprotective and therapeutic potential of baicalin, a flavonoid with known antioxidant, anti-inflammatory, and neurotropic properties, in an animal model of OCD induced by 8-OH-DPAT (8HPAT). The research utilized in silico docking studies and in vivo experiments to assess baicalin's interactions with key intracellular targets: SIRT-1, Nrf2, HO-1, and PPAR-gamma, and its effects on neurochemical, neurobehavioral, and histopathological parameters. In silico results indicated a strong binding affinity of baicalin for SIRT-1, Nrf2, HO-1, and PPAR-gamma, suggesting potential regulatory roles in antioxidant and anti-inflammatory pathways. In-vivo findings demonstrated that baicalin, administered at doses of 50 mg/kg and 100 mg/kg, significantly alleviated OCD-like behaviours, including excessive lever pressing, marble burying, and compulsive checking. Baicalin treatment normalized serotonin and dopamine levels and reduced glutamate levels in the brain, restoring neurotransmitter balance. Furthermore, baicalin decreased inflammatory cytokines (TNF-alpha and IL-1 beta), improved complete blood count profile, and gross morphological and histopathological alterations by restoring neuronal density and cellular integrity in affected brain regions. Combining baicalin with fluvoxamine (10 mg/kg) showed synergistic effects, further enhancing neuroprotective outcomes. These results suggest that baicalin holds promise as a potential therapeutic agent for OCD, warranting further clinical investigation to explore its efficacy and underlying mechanisms in human subjects. The findings underscore the importance of targeting intracellular pathways and neurotransmitter systems in developing effective treatments for OCD and related neuropsychiatric disorders.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578598"},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143738407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of clinical features of aquaporin-4 positive neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein associated disorder (MOGAD), and double seronegative NMOSD - A single center experience","authors":"Melike Cakan ,&nbsp;Ezgi Demirel ,&nbsp;Barışcan Cimen ,&nbsp;Nazire Pınar Acar Özen ,&nbsp;İlksen Çolpak ,&nbsp;Rana Karabudak ,&nbsp;Aslı Tuncer","doi":"10.1016/j.jneuroim.2025.578591","DOIUrl":"10.1016/j.jneuroim.2025.578591","url":null,"abstract":"<div><div>This retrospective study investigates Aquaporin-4 Antibody Positive Neuromyelitis Optica Spectrum Disorder (NMOSD), Myelin Oligodendrocyte Glycoprotein Associated Disorder (MOGAD), and Seronegative NMOSD at a tertiary care university hospital, over a 13 year period (November 2010 to November 2023) involving 78 patients. It distinguishes between the clinical and radiological features of AQP4 + NMOSD (41 patients, 52.5 %), MOGAD (22 patients, 28.2 %), and Seronegative NMOSD (15 patients, 19.3 %). A significant female majority was noted in AQP4+ NMOSD (90.2 %) compared to MOGAD (45.5 %) and Seronegative NMOSD (66.7 %). Age of disease onset and annualized relapse rates were similar across groups. Myelitis was a common initial symptom in AQP4+ NMOSD (48.8 %) and Seronegative NMOSD (40 %), but less so in MOGAD (18.2 %). Optic neuritis was more frequent in MOGAD (68.2 %) and Seronegative NMOSD (53.3 %) than AQP4+ NMOSD (31.7 %). Relapsing disease was less observed in MOGAD (57.1 %) compared to the other groups. Time to the first relapse varied: 12 months for Seronegative NMOSD, 18 months for AQP4+ NMOSD, and 7 months for MOGAD. A higher incidence of autoimmune disorders was found in AQP4+ NMOSD (36.6 %) versus MOGAD (9.5 %). This study delineates a pronounced female and concurrent autoimmune disorder predominance in AQP4+ NMOSD compared to seronegative NMOSD and MOGAD.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578591"},"PeriodicalIF":2.9,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143817238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ofatumumab for the treatment of COVID-19-associated autoimmune encephalitis: A case report","authors":"Zhuoran Wang ,&nbsp;Xiaoping Du ,&nbsp;Qiong Wang ,&nbsp;Yating Zhang ,&nbsp;Junhong Guo ,&nbsp;Huifang Wang","doi":"10.1016/j.jneuroim.2025.578590","DOIUrl":"10.1016/j.jneuroim.2025.578590","url":null,"abstract":"<div><div>Autoimmune encephalitis is a rare but severe complication of Coronavirus disease 2019 (COVID-19) infection. Typically, treatment involves immunomodulatory approaches such as steroids, intravenous immunoglobulin (IVIG), or plasma exchange. While for some patients, the above treatment is not effective. Here, we report a case of COVID-19-associated encephalitis, who exhibited cognitive impairment, epileptic seizures, tachycardia, and diaphoresis, with cranial MRI findings resembling those seen in limbic encephalitis. Initially, the patient exhibited a suboptimal response to antiviral therapy, high-dose steroids, and IVIG treatment. Nevertheless, his clinical symptoms and cranial MRI abnormalities markedly improved following the administration of Ofatumumab. Administering Ofatumumab early in COVID-19-related autoimmune encephalitis may benefit patients more.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578590"},"PeriodicalIF":2.9,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143706296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroinflammation and schizophrenia: The role of Toxoplasma gondii infection and astrocytic dysfunction","authors":"Abigail Everett,&nbsp;Hany M. Elsheikha","doi":"10.1016/j.jneuroim.2025.578588","DOIUrl":"10.1016/j.jneuroim.2025.578588","url":null,"abstract":"<div><div>Obligate intracellular pathogens such as the protozoan <em>Toxoplasma gondii</em> exploit host cell mechanisms to facilitate their survival and replication. While <em>T. gondii</em> can infect any nucleated mammalian cell, it exhibits a particular affinity for central nervous system cells, including neurons, astrocytes, and microglia. Among these, astrocytes play a pivotal role in maintaining neuroimmune balance, and their infection by <em>T. gondii</em> induces structural and functional alterations. Emerging evidence suggests that these changes may contribute to the pathophysiology of schizophrenia (SCZ). Although a direct causal link between <em>T. gondii</em>-induced astrocytic dysfunction and SCZ remains unproven, infection has been associated with increased kynurenic acid production, elevated dopamine levels, and heightened inflammatory cytokines—all of which are implicated in SCZ pathology. Additionally, <em>T. gondii</em> infection disrupts crucial neurobiological processes, including <em>N</em>-methyl-<span>d</span>-aspartate receptor signaling, blood-brain barrier integrity, and gray matter volume, further aligning with SCZ-associated neuropathology. This review underscores the need for targeted research into <em>T. gondii</em>-mediated astrocytic dysfunction as a potential factor in SCZ development. Understanding the mechanistic links between <em>T. gondii</em> infection, astrocytic alterations, and psychiatric disorders may open new avenues for therapeutic interventions.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"403 ","pages":"Article 578588"},"PeriodicalIF":2.9,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143696776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}