Neuroimmunomodulation最新文献

{"title":"Potential Microbiota-Immune-Neural Axis Mechanisms in Orthopedic Chronic Post-Surgical Pain.","authors":"Kourong Shi, Fancheng Chen, Lan Luo, Qiaoli Zhai, Huan Sun, Bingli Liu, Wei Fan","doi":"10.1159/nim/adxag013","DOIUrl":"https://doi.org/10.1159/nim/adxag013","url":null,"abstract":"<p><p>Chronic Post-Surgical Pain (CPSP) represents a prevalent complication following orthopedic surgery, significantly compromising patient recovery and quality of life. Emerging evidence indicates that the microbiota-immune-neural axis may play a contributory role in the pathogenesis and progression of CPSP, though direct causal evidence in patients undergoing orthopedic surgery remains limited. At the level of microbiota, gut dysbiosis may disrupt gut barrier integrity, potentially facilitating the translocation of bacterial products such as lipopolysaccharides into systemic circulation and thereby triggering systemic inflammatory responses. At the immunological level, microbial metabolites, particularly short-chain fatty acids, have been hypothesized to modulate the neuroimmune microenvironment through regulation of Treg/Th17 equilibrium. Activation of microglia and astrocytes may induce the release of pro-inflammatory cytokines, which may contribute to central sensitization. Concurrently, infiltration of peripheral immune cells at surgical sites may establish neuroinflammation, potentially resulting in persistent nociceptor activation. At the neural level, the vagus nerve and ascending spinal pathways constitute bidirectional communication conduits between the microbiota and brain. Gut dysbiosis may influence pain-modulating centers, including the amygdala and anterior cingulate cortex, via the gut-brain axis, thereby altering pain perception and emotional processing. It must be emphasized that much of the evidence discussed herein is indirect, associative, or derived from preclinical models, and should be interpreted accordingly. Therefore, in addition to introducing the proposed pathophysiology of CPSP, this review also presents possible microbiota-targeted intervention strategies and emphasizes the need for rigorous, orthopedically-specific randomized controlled trials before these strategies are implemented clinically.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216456","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":"Sweet Relief: Behaviorally conditioned analgesia in rats with inflammatory pain.","authors":"Stephan Leisengang, Lisa Trautmann, Yasmin Salem, Laura Lückemann, Kirsten Dombrowski, Julia Bihorac, Markus Leo, Linda-Isabell Schmitt, Sven Benson, Martin Hadamitzky, Manfred Schedlowski","doi":"10.1159/nim/adxag010","DOIUrl":"https://doi.org/10.1159/nim/adxag010","url":null,"abstract":"<p><p>The sensation of pain is modulated by a variety of physiological and psychological factors resulting in nocebo hyperalgesia and placebo analgesia. Modern pain therapy is increasingly regarded as a multimodal approach that combines pharmacological and non-pharmacological interventions. Associative-learning paradigms offer a promising adjunctive strategy for improving pain relief. To elucidate the neurobiological underpinnings, translation into an animal model is therefore warranted. Here, we aimed to apply a taste-associative learning paradigm in a model of inflammatory pain to induce a state of conditioned analgesia in rats. Male Dark Agouti rats received an intraplantar injection of Complete Freund's adjuvant (CFA) to elicit inflammatory pain; ibuprofen (100 mg/kg) was used as analgesic. Pain-associated behavioral changes were assessed in an open field test, Von Frey test, and Plantar Heat test. For the conditioning experiments, treatment with ibuprofen as unconditioned stimulus (US) was paired to the presentation of a sweet taste of saccharin (conditioned stimulus; CS) on days 2, 4, and 6 after CFA-injection (acquisition). On day 8, conditioned responses were evoked by presenting saccharin followed by a placebo injection (retrieval). CFA induced clear behavioral adaptations, including reduced water intake, weight loss, diminished locomotor activity, and lower mechanical and thermal withdrawal thresholds. Spontaneous pain-associated behaviors returned to baseline from day 2 post-CFA, whereas stimulus-evoked behaviors remained attenuated throughout the experiment. Treatment with ibuprofen markedly raised withdrawal thresholds, confirming its analgesic effect. Pairing ibuprofen (US) with saccharin (CS) produced a conditioned taste avoidance (CTA). Rats that had undergone the conditioning displayed conditioned analgesia, evidenced by elevated thermal and mechanical withdrawal thresholds compared to the non-conditioned vehicle group. Our results demonstrate that a state of conditioned analgesia can be induced in rats using a taste-associative learning paradigm. Consequently, our model constitutes a valuable tool for further investigating the neurobiological mechanisms involved in placebo-mediated analgesia.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149168514","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":"Peripheral CCK and ß-Endorphin as Potential Neuroendocrine Markers of Nocebo Effects: Evidence from a Multiple-Threat Pain Paradigm.","authors":"Alex Köhler, Harald Engler, Robert Jan Pawlik, Anna Ceylan, Julian Kleine-Borgmann, Sigrid Elsenbruch, Jana L Aulenkamp","doi":"10.1159/nim/adxag011","DOIUrl":"https://doi.org/10.1159/nim/adxag011","url":null,"abstract":"<p><strong>Introduction: </strong>Nocebo effects are shaped by negative treatment-related expectations and experiences and can contribute to adverse treatment outcomes. They have been linked to neuroendocrine alterations, yet reliable peripheral biomarkers remain elusive. Although cholecystokinin (CCK) has long been implicated in nocebo hyperalgesia, direct evidence in humans remains limited. β-Endorphin (β-END) is another promising candidate given its established role in endogenous pain modulation and placebo analgesia. The present study aimed to investigate whether peripheral CCK and β-END responses are associated with nocebo effects in the visceral pain modality.</p><p><strong>Methods: </strong>In this biomarker-focused analysis of the experimental NOVIS trial, healthy volunteers (N = 100) underwent a multiple-threat pain paradigm comprising visceral (rectal distension) and somatic (cutaneous heat) pain stimulation. Participants were randomized to receive negative versus neutral verbal treatment suggestions and either an adverse or a neutral treatment experience. Plasma concentrations of CCK and β-END were assessed during the treatment phase (T1), after the treatment phase (T2), and following the subsequent test phase (T3). Visceral pain unpleasantness ratings served as the primary behavioral measure of nocebo responding. Generalized linear mixed models were used to examine between-group differences in neuroendocrine responses, responder versus non-responder differences based on nocebo-induced changes in visceral pain unpleasantness, and exploratory sex differences.</p><p><strong>Results: </strong>For CCK, between-group analyses yielded no significant differences. The post-hoc responder analysis revealed that nocebo responders exhibited significantly higher peripheral CCK concentrations during treatment (T1) compared to non-responders, with no differences at subsequent time points. Women exhibited significantly higher β-END concentrations than men across all groups and time points, with no nocebo-related group differences or changes observed.</p><p><strong>Conclusion: </strong>Elevated CCK concentrations during treatment may constitute a dispositional marker of nocebo susceptibility or an early anticipatory neuroendocrine response to treatment-related interpersonal cues. Higher β-END in women may reflect sex-related variation in peripheral opioid-associated neuroendocrine responses rather than a nocebo-specific mechanism. These findings may inform future efforts to identify biological and contextual factors that shape nocebo susceptibility and, ultimately, to develop more individualized communication strategies in clinically vulnerable populations such as persons living with chronic visceral pain in disorders of gut-brain interactions.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149167951","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":"The Tumor Neuroimmune Niche: A Unifying Framework for Cancer Progression and Its Neuropsychiatric Burden.","authors":"Agastya Mittal, Clayton Rawson, Jaime Tellez, Chibeze Oguejiofor, Ziya Karimov, Jerick Kim, Brandon Lucke-Wold, Michael Karsy, Mehrdad Pahlevani","doi":"10.1159/nim/adxag012","DOIUrl":"https://doi.org/10.1159/nim/adxag012","url":null,"abstract":"<p><strong>Background: </strong>Cancer has traditionally been framed as a cell-intrinsic genetic disease and, more recently, as a disorder of the tumor microenvironment (TME). An emerging third view reframes malignancy as a systems-level neuroimmune disorder, in which neurons, glia, immune cells, and tumor cells form a continuously communicating network, the tumor neuroimmune niche.</p><p><strong>Summary: </strong>This review synthesizes evidence that the nervous system actively regulates tumor initiation, proliferation, angiogenesis, invasion, and metastasis through autonomic, sensory, and neuroendocrine inputs, while tumors in turn remodel both peripheral nerves and central circuits. Sympathetic, parasympathetic, and sensory fibers shape the immune compartment, frequently driving T-cell exhaustion, macrophage repolarization, and an immunosuppressive milieu via β-adrenergic and neuropeptide signaling. The immune system operates as a central mediator of this dialogue: cytokines such as interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α) relay tumor-derived signals to the brain through neural and humoral routes, activating the same circuits that produce sickness behavior, fatigue, depression, and cognitive impairment. These neuropsychiatric sequelae are common, durable, and poorly explained by tumor stage alone, positioning the central nervous system (CNS) at the center of the disease rather than at its periphery. Cancer therapies, chemotherapy, immune checkpoint inhibitors (ICIs), and radiation, further perturb the neuroimmune axis and contribute to lasting neurotoxicity. Translational opportunities include neuroimmune biomarkers, neural-activity signatures, and the repurposing of β-blockers, vagus nerve stimulation (VNS), and neurotransmitter-targeted agents as antitumor strategies.</p><p><strong>Key messages: </strong>The circuits driving tumor progression and those producing the neuropsychiatric burden of cancer may substantially overlap. Integrating cancer neuroscience, immuno-oncology, and psycho-oncology is essential to convert this biology into therapy. Recognizing cancer as a neuroimmune disease opens a roadmap toward targeting the nervous system as a modifiable axis of oncologic care.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128198","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":"Peripheral and central neuroinflammatory mechanisms regulating vagal sensory circuit processing and cough in lung disease.","authors":"Stuart B Mazzone, Alexandria K Driessen, Nathalie A J Verzele","doi":"10.1159/nim/adxag009","DOIUrl":"https://doi.org/10.1159/nim/adxag009","url":null,"abstract":"<p><strong>Background: </strong>The pulmonary system can be exposed to a diverse range of injurious insults which drive pathological events including inflammation, tissue damage and structural remodelling within the airways and lungs.</p><p><strong>Summary: </strong>Patients with lung inflammation and injury often experience sensory neurological complications, suggesting that the pathological processes in the lung either impact or extend into the nervous system.</p><p><strong>Key messages: </strong>Cough is a common presenting neurological symptom in patients with lung disease and there is growing evidence that neuroinflammation, either within the vagal nerves innervating the airways and lungs or within the central sensory neural circuits regulating cough, is involved in the development of cough disorders. We review and summarise the evidence that lung inflammation and injury drive regional neuroinflammation along peripheral and central vagal sensory pathways, co-ordinated by inflammatory cell recruitment and activation, resulting in altered gene and protein expression, vascular disruption and neurophysiological changes. We also discuss the current therapies in development for chronic cough and highlight the need to consider disease modifying therapeutics that target neuroinflammation.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081700","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":"Towards a Cortical Framework of Neuroimmune Representation: The Insular Cortex at the Brain-Immune Interface.","authors":"Julia Bihorac, Martin Hadamitzky","doi":"10.1159/nim/adxag008","DOIUrl":"https://doi.org/10.1159/nim/adxag008","url":null,"abstract":"<p><strong>Background: </strong>For a long time, the immune system was considered as an autonomous defense network. The possibility that its functional states are actively represented and regulated at the cortical level challenges this dogma and demands a reconceptualization of immunity as a brain-orchestrated process. Especially, the insular cortex is uniquely positioned to represent internal physiological states and to exert top-down control over peripheral immune responses. Within the insular cortex, interoceptive stimuli are transformed into integrated representations of bodily states. Through projections to the hypothalamus and the brainstem, the insular cortex influences autonomic and neuroendocrine outputs, enable context-dependent modulation of systemic cytokine production and immune cell activity. Importantly, recent findings suggest that previous immune experiences are not only stored as neuronal engrams within insular cortical circuits but can also be reinstated upon selective reactivation. This perspective discusses the role of the insular cortex as a central hub within a dynamic, network linking interoceptive and cortical processes with immunity.</p><p><strong>Summary: </strong>Beyond its role in bidirectional neuroimmune regulation, the insular cortex has been proposed to function as a cortical hub for encoding immune-state representations.</p><p><strong>Key message: </strong>Resolving where and how the brain encodes peripheral immune states will not only illuminate how central dysregulation contributes to disease, but may reveal new therapeutic targets in which experiential and cognitive variables become tractable levers for immune intervention.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149039888","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":"Temporal Dynamics in Neuroimmunomodulation and Aging: Moving Beyond Snapshot Biology.","authors":"Alexander K H Weiss","doi":"10.1159/nim/adxag007","DOIUrl":"https://doi.org/10.1159/nim/adxag007","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148983354","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":"Associations of a Pre-Chemotherapy Anxiety-Sleep Disturbance Phenotype with Cellular Immunity and Quality of Life in Colorectal Cancer Patients: Statistical Mediation by Cortisol and IL-6.","authors":"Xujin Guo, Xiao Wang, Yuping Song, Qian Bao, Lina Cheng, Haina Wu, Ya Feng, Fang Chen","doi":"10.1159/nim/adxag002","DOIUrl":"10.1159/nim/adxag002","url":null,"abstract":"<p><strong>Background: </strong>Neuroimmunomodulation examines nervous-immune interactions via hormonal and inflammatory pathways. This study investigated whether the anxiety-sleep disturbance symptom cluster in colorectal cancer (CRC) patients undergoing chemotherapy is associated with neuroendocrine dysregulation, cellular immune alterations, and quality of life (QoL), and tested whether cortisol and interleukin-6 (IL-6) act as biological mediators.</p><p><strong>Methods: </strong>In this prospective baseline observational study, 268 CRC patients scheduled to initiate systemic chemotherapy were assessed within 24 hours before their first chemotherapy cycle. Anxiety (HADS-A), sleep quality (PSQI), and QoL (EORTC QLQ-C30) were assessed. Serum cortisol, IL-6, and TNF-α were quantified by ELISA. Lymphocyte subsets (CD3+, CD4+, CD8+, NK cells) and regulatory T cells (Tregs) were analyzed by flow cytometry. Patients with HADS-A ≥8 and PSQI >5 formed the Symptom Cluster group (n=118), while the remaining patients constituted the Non-cluster comparator group (n=150). Mediation analysis using bootstrapping tested cortisol and IL-6 as intermediaries.</p><p><strong>Results: </strong>The Symptom Cluster group showed significantly elevated cortisol, IL-6, and TNF-α (all P<0.001), higher Treg proportion (8.4% vs. 4.6%, P<0.001), and lower CD3+, CD4+, and NK cell counts (all P<0.001). Global QoL was reduced (36.4 vs. 69.5, P<0.001). Cross-sectional mediation models indicated that the association between symptom-cluster status and CD4+ T-cell count was statistically mediated by cortisol (indirect effect, -117.45; 95% bootstrap CI, -168.22 to -75.40), and the association with global QoL was statistically mediated by IL-6 (indirect effect, -13.85; 95% bootstrap CI, -18.50 to -9.80), accounting for 37.9% and 41.8% of the total effects, respectively.</p><p><strong>Conclusion: </strong>The anxiety-sleep disturbance symptom cluster in CRC chemotherapy patients is associated with neuroendocrine-inflammatory dysregulation, effector immune suppression, Treg expansion, and impaired QoL. Exploratory mediation findings suggest that cortisol and IL-6 may be involved in statistical indirect associations between this pre-chemotherapy anxiety-sleep disturbance phenotype and immune/QoL outcomes; longitudinal studies are needed to determine temporal and causal relationships.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1"},"PeriodicalIF":3.7,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897467","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":"The Participation of Prolactin in the Immunopathology of Experimental Pulmonary Tuberculosis.","authors":"Dulce Adriana Mata-Espinosa, Gabriel Quintero-Bustos, Daniel Enrique Castillo Baltazar, Blanca Estela Tovar-Vázquez, Jorge Alberto Barrios-Payán, Rogelio Hernández-Pando","doi":"10.1159/000552692","DOIUrl":"10.1159/000552692","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Prolactin and its receptor are widely recognized for their roles in lactogenesis and galactopoiesis. However, they have also gained attention for their role in immune pathophysiology, acting as mediators of both innate and acquired immune responses and potentially playing a significant role in chronic infectious diseases such as tuberculosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;In this study, we examined the kinetics of prolactin and its receptor during the progression of experimental pulmonary tuberculosis in BALB/c mice infected intratracheally with a high-dose Mycobacterium tuberculosis (M. tuberculosis) reference strain, H37Rv. Groups of infected mice were euthanized at various time points, and their lungs were collected to quantify gene expression of prolactin and its receptor by RT-PCR, as well as to assess cellular expression by immunohistochemistry. In vitro infection experiments with alveolar macrophages and type II pneumocyte cell lines were conducted to evaluate the effects of prolactin on bacteriolysis and the expression of various innate immune response factors. After 2 months of infection, BALB/c mice with progressive pulmonary tuberculosis were treated with ovine PRL, and the effects were assessed by measuring bacillary loads and the extent of tissue damage (pneumonia).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;In vitro studies showed that prolactin increases bacterial phagocytosis in alveolar macrophages and significantly enhances the production of reactive oxygen and nitrogen species, which reduces bacillary loads. In type II pneumocytes, prolactin, under certain conditions, induces higher, though not statistically significant, expression of cathelicidin and surfactant proteins A and D. In vivo studies revealed that, during early infection (within the first week), there was high expression of prolactin and its receptor in the lungs. Immunostaining for prolactin and its receptor was observed at the early stage of infection, mainly in alveolar epithelial cells, macrophages, and lymphocytes. During the second week of infection, immunostaining showed the organization of macrophages and lymphocytes within granulomas and in the inflammatory infiltrate around blood vessels and airways, with macrophages showing the strongest staining. Over the course of progressive disease, after 1 month of infection, pulmonary prolactin production decreased, and some macrophages and lymphocytes showed minimal prolactin immunostaining, although high prolactin receptor expression persisted; 4 months later, prolactin immunostaining was observed in the bronchial epithelium. Administration of prolactin via intraperitoneal injection 2 months after infection resulted in a significant reduction in bacillary loads after 2 months of treatment, along with increased but not statistically significant expression of TNFα and IFNγ.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Prolactin and its receptors appear to contribute to immune activation during pulmon","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"288-299"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148055962","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":"A Comprehensive Review of Worldwide Case Series of Neurocysticercosis and Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis.","authors":"Iris E Martínez-Juárez, Santiago Philibert-Rosas, Irving Fuentes-Calvo, Jimena Gonzalez-Salido, Luis A Marin-Castañeda, Jimena Colado-Martinez, Jimena Armenta-Báez, Andrea Michell Peralta-Maza, Mario A Sebastián-Díaz, Karen Guzmán-Sánchez, Betsy C Vázquez-Cruz, Fernando Vasquez-Lopez, Andrea Santos-Peyret, Aurelio Jara-Prado, Adriana Ochoa-Morales, Salvador Martínez-Medina, Fernando Sotelo-Díaz, Agnès Fleury, Jorge G Burneo, Julio Sotelo","doi":"10.1159/000552190","DOIUrl":"10.1159/000552190","url":null,"abstract":"<p><strong>Background: </strong>Neurocysticercosis (NCC) is a frequent cause of epilepsy in endemic regions. An association between NCC and hippocampal sclerosis (HS), a key pathological substrate of mesial temporal lobe epilepsy, has been increasingly reported but remains controversial.</p><p><strong>Summary: </strong>A literature search was conducted in PubMed, Scopus, and ScienceDirect focusing on publications describing epilepsy due to NCC with HS. Twenty-three original articles, identified through 2023, were retrieved from Brazil, Ecuador, India, Mexico, and Korea. The proposed relationships between NCC and HS include incidental coexistence, NCC as an initial precipitating injury, and the presence of a third variable. While multiple hypotheses have been discussed and reported cases compiled, the precise nature of this association remains unresolved.</p><p><strong>Key messages: </strong>Although the mechanisms underlying the relationship between NCC and HS are not fully elucidated, evidence supports their coexistence in patients with epilepsy. Recognition of this association is important for clinical evaluation and may guide future research on pathogenesis and management.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"225-235"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13327664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777277","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}