Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology最新文献

{"title":"Efficacy and Safety of Adjunctive Minocycline in the Treatment of Autoimmune Encephalitis (MEET): A Proof of Concept Study.","authors":"Yingchi Zhang, Jingjing Zhao, Zhirong Fan, Xiaomu Wang, Xiaodan Shi, Xuan Wang, Ting Wan, Fang Du, Kejian Wu, Wen Jiang","doi":"10.1007/s11481-026-10290-1","DOIUrl":"10.1007/s11481-026-10290-1","url":null,"abstract":"<p><p>BACKGROUND: This study aims to determine whether 4 weeks of adjunctive minocycline can improve cognitive and neurological symptoms in patients with autoimmune encephalitis (AE). METHODS: In this randomized, open-label, blinded-endpoint trial, participants were randomized (1:1) to receive first-line immunotherapy with or without minocycline (100 mg twice daily for 4 weeks). Clinical outcomes included changes in the Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE), Hamilton Anxiety Rating Scale (HAMA), Hamilton Depression Rating Scale (HAMD), modified Rankin Scale (mRS), and Clinical Assessment Scale in Autoimmune Encephalitis (CASE). The exploratory outcome was the change in Soluble Triggering Receptor Expressed on Myeloid cells 2 (sTREM2), a biomarker of microglial activation. Follow-up assessments were conducted at weeks 4, 12, 24, and 48. RESULTS: Sixty patients with AE were enrolled. For the primary outcome, the difference in mean change in MoCA scores between the groups was 1.05 (P = 0.46) from baseline to week 12. However, at week 4, the minocycline group demonstrated significantly improvements in MoCA (difference, 3.85; 95% CI, 1.04 to 6.66; P = 0.008) and MMSE (difference, 3.23; 95% CI, 0.20 to 6.26; P = 0.037) compared to the control group. CSF sTREM2 levels decreased in the minocycline group (difference, –93.3; 95% CI, –186.60 to –0.05; P = 0.050). No other secondary outcomes differed between groups. Adverse events were mild, and no allergic reactions were reported. CONCLUSIONS: Adjunctive minocycline for 4 weeks showed a significant improvement in cognitive performance. However, no sustained benefits were observed beyond the treatment period. CLINICAL TRIALS REGISTRATION: NCT06033846. </p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147576900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"5,7,4'-Trimethoxyflavone Attenuates Cognitive Impairment in Diabetic Mice via Inhibition of NLRP3 Inflammasome Activation.","authors":"Maryam N ALNasser, Peramaiyan Rajendran","doi":"10.1007/s11481-026-10291-0","DOIUrl":"10.1007/s11481-026-10291-0","url":null,"abstract":"<p><p>Diabetic encephalopathy is a severe consequence of diabetes mellitus characterised by cognitive deterioration. Neuroinflammation is pivotal in the pathophysiology of this illness. This study examined the efficacy of 5,7,4′-trimethoxyflavone (TMF) in modulating neuroinflammation to mitigate cognitive deficits in streptozotocin (STZ)-induced diabetic mice. Diabetes was induced in male mice through STZ administration before treatment with TMF. Cognitive function was evaluated using the Morris water maze and Y-maze tests. Brain tissue was examined for indicators of oxidative stress, including superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA). The expression levels of critical neuroinflammatory components – including the NLR family pyrin domain containing 3 (NLRP3) inflammasome and its apoptosis-associated Speck-like protein containing a CARD (ASC) – together with the downstream cytokines interleukin-1 beta (IL-1β) and interleukin-18 (IL-18), were assessed. In addition, the concentrations of brain-derived neurotrophic factor (BDNF), cleaved caspase-1, glial fibrillary acidic protein (GFAP), and neuron-specific nuclear protein (NeuN) were measured. TMF treatment markedly boosted cognitive function in diabetic mice, as reflected by improved spatial learning and memory in the Morris water maze and superior working memory performance in the Y-maze. Moreover, TMF treatment diminished oxidative stress, as evidenced by elevated SOD and CAT activity and decreased MDA levels. TMF markedly inhibited the activation of the NLRP3 inflammasome by diminishing the expression of NLRP3 and ASC, thereby reducing the levels of IL-1β and IL-18. Furthermore, TMF therapy elevated BDNF levels and decreased cleaved caspase-1 expression, indicating neuroprotective properties. Immunohistochemistry demonstrated that TMF reduced GFAP expression and elevated NeuN expression in the hippocampus. The results collectively indicate that TMF provides neuroprotection and mitigates cognitive deficits in STZ-induced diabetic mice, effectively suppressing neuroinflammation and oxidative stress pathways in a dose-dependent manner. Consequently, TMF holds potential as a treatment for diabetic encephalopathy.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147522864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanisms of Mangiferin on Neuroinflammation for Treating Major Depressive Disorder Based on Network Pharmacology and Bioinformatics Analysis.","authors":"Cong-Ya Chen, Lan Lei, Xuan Yang, Yu-Fei Wang, Yi Zhang","doi":"10.1007/s11481-026-10282-1","DOIUrl":"10.1007/s11481-026-10282-1","url":null,"abstract":"<p><p>Major depressive disorder (MDD) is a heterogeneous disease with complex etiology, accompanied by high morbidity and disability. Recently, neuroinflammation has been identified as a crucial mechanism in major depressive disorder. Mangiferin (MGF) is a natural flavonoid polyphenolic compound primarily extracted from Anemarrhenae Rhizome or mango that exhibits promising anti-inflammatory activity in the preclinical treatment of MDD. The present research used network pharmacology and bioinformatics to identify 3 core targets (ICAM1, MAPK3, and MMP9) associated with MGF for treating neuroinflammation in MDD. We have identified MDD as being closely associated with immunity and neuroinflammation, with core targets primarily related to calcium and the NOD-like receptor signaling pathway, among others. Based on molecular docking studies, MGF has good binding activity with MAPK and MMP9. This research suggests that MGF has the potential to treat neuroinflammation in MDD, providing a basis for further exploration of its clinical application in treating neuroinflammation associated with MDD.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147461293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling.","authors":"Zhenzhao Luo, Deyong Kong, Guangjian Qi, Chao Zheng, Wushi Zhao, Zhongxin Lu","doi":"10.1007/s11481-026-10284-z","DOIUrl":"10.1007/s11481-026-10284-z","url":null,"abstract":"<p><p>Formyl peptide receptor-2 (FPR2) belongs to the G protein-coupled receptor (GPCR) family and plays a critical role in the development of various tumors. However, the roles and mechanisms of FPR2 in glioblastoma (GBM) remain poorly understood. In this study, we observed significant upregulation of FPR2 in glioma cell lines and tissues, and elevated FPR2 expression levels are correlated with poor patient survival. Furthermore, we found that FPR2 suppresses the autophagy mediated by BECN1 and ATG5 in GBM cells. Using Western blot analysis, we revealed that FPR2 regulates GBM cell invasion via the PI3K/AKT signaling pathway. Additionally, we demonstrated that knocking down FPR2 expression in GBM cells reduced tumor cell migration and invasion in vitro and tumor growth in vivo. The inhibition of FPR2 led to cell cycle arrest at the G2/M phase and increased apoptosis. Finally, our findings indicate that FPR2 may prevent autophagy-induced epithelial‒mesenchymal transition (EMT)-like changes by preventing autophagy-induced degradation of Snail. Our findings suggest that FPR2 promotes GBM cell migration and invasion through the inhibition of autophagy and the activation of the PI3K/AKT signaling pathway, highlighting the potential of inducing autophagy as a therapeutic approach to inhibit invasion in GBM with high FPR2 expression.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147391811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin Mitigates Central Sensitization and Nociplastic Pain in Spinal Cord and Dorsal Root Ganglia of FM Rat Model: Modulation of SIRT1/PGC-1α/MAPK/NF-κB Signaling.","authors":"Jehad Osama, Amira A El-Gazar, Ghada M Ragab, Nesrine S El-Sayed, Ahmed S Kamel","doi":"10.1007/s11481-025-10274-7","DOIUrl":"10.1007/s11481-025-10274-7","url":null,"abstract":"<p><p>Fibromyalgia (FM) is a central sensitization syndrome characterized by neuroinflammation and synaptic hyperexcitability, which amplifies pain signals in the spinal cord (SC) and dorsal root ganglia (DRG). Melatonin (MEL) has demonstrated analgesic and antinociceptive properties in experimental models, supporting its clinical application in various pathological conditions. This study aimed to elucidate the impact of Melatonin on neuroinflammation and glutamatergic dysregulation in the spinal cord and DRG using a Reserpine-induced fibromyalgia model (RIFM). RIFM was induced in female rats by administering Reserpine (1 mg/kg/day, s.c.) for three consecutive days. Melatonin (10 mg/kg, orally) was administered for three days following the peak of pain on day 7. Melatonin significantly ameliorated stimulus-evoked pain in thermal and mechanical tests, with a resolution of spontaneous pain noted by the rat grimace scale. Moreover, motor activity in the open field task and depressive behavior in the tail suspension test (TST) were alleviated following Melatonin administration. Fibromyalgia pain was associated with enhanced glutamatergic transmission, as shown by immunohistochemical assessment of synaptophysin and PSD95 in the DRG along with VGLUT, PSD95, NMDA, NMDA receptor 2B, and AMPA in the spinal cord. Reserpine-induced disturbances in mitochondrial biogenesis markers, SIRT1 and PGC-1α, were followed by an upsurge of TNF-α, NFkB, and P38-MAPK. This neuroinflammatory milieu was marked by elevated ionized calcium-binding adaptor molecule-1 (Iba-1) in activated microglia within the spinal cord. These pathological findings were notably mitigated by Melatonin, as reflected by increased expressions of spinal MT1 and MT2 receptors. In conclusion, Melatonin exhibited antinociceptive and anti-inflammatory effects by modulating glutamate neurotransmission, mitochondrial dysfunction, and microglial activation, thereby alleviating nociplastic pain in the experimental RIFM.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"12"},"PeriodicalIF":3.5,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12904926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146183638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EcoHIV Infection Disrupts Dopamine and Serotonin Transporter Function, Altering Release Dynamics in C57BL/6J Mice.","authors":"Jun Zhu, Carles Moreno, Ana C Jimenez Torres, Sarah E Davis, Abagail B Cirincione, Sanjay B Maggirwar","doi":"10.1007/s11481-026-10280-3","DOIUrl":"10.1007/s11481-026-10280-3","url":null,"abstract":"<p><p>The long-term expression of neurotoxic viral proteins within the central nervous system plays a critical role in the neuropathology associated with HIV-1, particularly in the development of HIV-1 associated neurocognitive disorders. This hypothesis is predominantly supported by findings from rodent models exposed to the HIV-1 transactivator of transcription (Tat) protein, which exhibit disruptions in monoamine transmission that correlate with cognitive deficits. However, previous studies have often overlooked the complex interactions among other viral proteins. To address this gap, we utilized a novel EcoHIV-infected mouse model designed to elucidate the nuances of monoamine transmission and function. EcoHIV, a chimeric virus with the HIV-1/NL4-3 gp120 coding region replaced by gp80 from ecotropic MuLV-1, facilitates infection in mice and serves as an innovative platform for NeuroHIV research. Results reveal that EcoHIV infection in C57BL/6J mice leads to increased dopamine transporter-mediated dopamine uptake in the prefrontal cortex, while simultaneously reducing serotonin transporter-mediated serotonin uptake in the hippocampus. Fast-scan cyclic voltammetry demonstrated augmented dopamine release in the nucleus accumbens paired with normal release levels in the caudate putamen, contrasted by a significant reduction in serotonin release from the substantia nigra. These alterations were accompanied by heightened horizontal activity in EcoHIV-infected mice. Immunohistochemistry and immunofluorescence analyses further revealed reductions in synaptic density and integrity, alongside microglial activation in the affected brain regions. This research offers crucial insights into the neuropathological progression of HIV-associated neurocognitive and depressive disorders, aligning with clinical evidence observed in people living with HIV and paving the way for potential therapeutic interventions.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"11"},"PeriodicalIF":3.5,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12894441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146159550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beta-lactam Antibiotic Cefepime Attenuates Lipopolysaccharide-induced Pain and Depression By Modulating Inflammatory Response and Astroglial Glutamate Transporter in Mice.","authors":"Amna Khan, Patrick J Ronan, Shafiqur Rahman","doi":"10.1007/s11481-026-10279-w","DOIUrl":"10.1007/s11481-026-10279-w","url":null,"abstract":"<p><p>Emerging evidence suggests that the brain glutamatergic system has a critical role in the pathophysiology of comorbid pain and depression. Cefepime is a widely used fourth-generation beta-lactam cephalosporin antibiotic and it has been shown to have neuroprotective properties in various animal models. In this study, cefepime is hypothesized to exert anti-nociceptive, anti-depressant, anxiolytic, and procognitive-like effects by modulating microglial activation and excessive glutamatergic neurotransmission in mice. Therefore, we have investigated the effects of cefepime on tactile allodynia, thermal hyperalgesia, depression, anxiety, and cognitive deficit-like behaviors in a mouse model of comorbid pain-depression induced by LPS. In addition, we have determined the effects of cefepime on astroglial expression of GLT-1 and microglial expression of Iba-1 in the hippocampus and prefrontal cortex using the Western blot analysis. We also evaluated the effects of cefepime on TNF-α and IL-1β levels in the hippocampus and prefrontal cortex using ELISA. Our results demonstrated that cefepime (50 mg/kg and 200 mg/kg i.p.) significantly attenuated LPS-induced nociceptive pain, depression, anxiety, and cognitive deficit-like behaviors in mice. In contrast, selective blockade of astroglial GLT-1 with dihydrokainic acid (10 mg/kg i.p.) significantly abolished the anti-nociceptive, anti-depressant, anxiolytic, and procognitive-like effects of cefepime (200 mg/kg i.p.), suggesting that these effects are mediated by the astroglial GLT-1 transporter. Western blot analysis indicated that cefepime (200 mg/kg) significantly reversed the LPS-reduced GLT-1 expression in the hippocampus and prefrontal cortex. Moreover, cefepime (200 mg/kg) effectively modulated the LPS-induced microglial activation as evidenced by decreased expression of Iba-1 in the hippocampus and prefrontal cortex. Notably, cefepime (200 mg/kg) significantly prevented the LPS-induced increased TNF-α and IL-1β levels in the hippocampus and prefrontal cortex by targeting glial mechanisms. Overall, these results suggest that novel glutamate transporter modulator cefepime could be developed as potential therapeutic utility for comorbid pain and depression.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"10"},"PeriodicalIF":3.5,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146108950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-dose IL-2 Ameliorates Experimental Autoimmune Myasthenia Gravis in Rats by Restoring the CD4-positive Helper T-cell Balance Via the JAK/STAT5 Pathway.","authors":"Shanshan Peng, Xiaotong Kong, Wenqi Tian, Fanfan Xu, Hanlu Cai, Fei Wu, Ying Li, Guanghao Xin, Jingyan Niu, Yingjie Ren, Lei Li, Jianjian Wang, Huixue Zhang, Lihua Wang","doi":"10.1007/s11481-025-10276-5","DOIUrl":"10.1007/s11481-025-10276-5","url":null,"abstract":"<p><p>Myasthenia gravis (MG) represents a prototypical autoimmune disorder that targets neuromuscular junctions. Emerging insights into the pathogenic role of cellular immunity in MG have intensified investigations of potential immunomodulatory therapies, and low-dose interleukin-2 (LD-IL-2) has garnered particular attention because of its ability to restore immune balance, maintain immune homeostasis, and ensure immune tolerance. To systematically investigate the therapeutic potential of LD-IL-2 in MG and elucidate its underlying mechanisms, we established an experimental autoimmune myasthenia gravis (EAMG) rat model to assess its therapeutic effects on clinical manifestations and CD4-positive helper T (CD4+ T) cell subset differentiation. Through integrated in vivo and in vitro experiments, we conducted a comprehensive evaluation of the immunoregulatory properties of LD-IL-2 in the context of EAMG pathogenesis. Our results revealed a pronounced imbalance in CD4+ T cells in EAMG model rats. Our research confirmed that LD-IL-2 might restore the Th17/regulatory T (Treg) cell and T follicular helper (Tfh)/T follicular regulatory (Tfr) cell ratios, thereby reestablishing the balance of CD4+ T cells in the EAMG model and improving the clinical severity of EAMG in rats. Moreover, we demonstrated that LD-IL-2 might exert its effects by activating the JAK1/JAK3/STAT5 signaling pathway and modulating CD4+ T cell differentiation. Collectively, our research provides compelling evidence supporting LD-IL-2 as a viable immunotherapeutic candidate for MG, laying a robust experimental foundation for future clinical applications in MG patients.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"9"},"PeriodicalIF":3.5,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146094992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploratory Cohort Study of Depressive Symptoms in South Africans with HIV-1 Subtype C: Associations with Kynurenine Pathway Metabolites and Inflammatory Markers.","authors":"Monray Edward Williams, Lusilda Schutte, Levanco K Asia, Marié P Wissing, Esmé Jansen van Vuren","doi":"10.1007/s11481-025-10278-3","DOIUrl":"10.1007/s11481-025-10278-3","url":null,"abstract":"<p><p>Background: Depression is common in people living with HIV and may involve immune–metabolic dysregulation. Altered tryptophan (Trp) metabolism via the kynurenine (Kyn) pathway, particularly quinolinic acid (QUIN), has been linked to neuroinflammation and depression, yet data from South Africans with HIV-1 subtype C are limited. Methods: In this exploratory cohort, treatment-naïve adults with HIV were assessed at baseline in 2010 (n = 69) and followed up in 2015 (n = 40). Targeted LC-MS/MS quantified Trp–Kyn metabolites (Trp, Kyn, KA, QUIN) and ELISAs measured immune markers (suPAR, IL-6, hsCRP, sCD163, NGAL). Depressive symptoms were evaluated using the PHQ-9 at baseline and follow-up. Results: Baseline QUIN was associated with the PHQ-9 total score (adjusted R²=0.245; β=0.417; p = 0.004, p(Hochberg) = 0.044) and also increased odds of depression risk (OR=61.1; 95%CI 2.24–1664.76; p = 0.015, p(Hochberg) = 0.030) at baseline. Baseline NGAL was significantly lower in the follow-up group with self-harm thoughts compared to the group with no–self-harm thoughts (p = 0.008) and lower NGAL predicted greater odds of follow-up self-harm thoughts (OR = 0.007, 95% CI: <0.001–0.572, p = 0.027, p(Hochberg) = 0.027). When PHQ-9 subscales were examined, baseline QUIN, Kyn, hsCRP, and suPAR showed positive associations with the baseline somatic subscale (β range= 0.34–0.57, all p < 0.01), whereas the baseline cognitive–affective subscale was not associated with any marker. No baseline markers were associated with follow-up depression risk or scores. Over five years, suPAR decreased whereas hsCRP did not change significantly, however changes in these markers over time did not reveal any associations with the PHQ-9 total or subscale scores. Conclusions: In this exploratory cohort, higher peripheral QUIN may be linked to depression risk, particularly with somatic rather than cognitive–affective symptom dimensions. Lower baseline NGAL was the only marker associated with later self-harm thoughts, suggesting a potential neuroimmune signal that warrants further investigation. Larger, adequately powered longitudinal studies with repeated metabolomic assessments are warranted to confirm this finding and clarify temporal and causal relationships between immune–metabolic dysregulation and specific depressive symptom profiles.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"8"},"PeriodicalIF":3.5,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12830437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146031909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: PKR Inhibition Prevents Neuroinflammation and Rescues Depressive‑Like Behaviors Via BDNF/TrkB Signaling.","authors":"Yue Hu, Tahir Ali, Shengnan Mou, Qichao Gong, Ruyan Gao, Yanhua Luo, Shupeng Li, Li Ling, Liangliang Hao","doi":"10.1007/s11481-025-10277-4","DOIUrl":"10.1007/s11481-025-10277-4","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"7"},"PeriodicalIF":3.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145992298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}