Brain, behavior, & immunity - health最新文献

{"title":"Impact of social isolation during the COVID-19 pandemic on the mental health of university students and recommendations for the post-pandemic period: A systematic review","authors":"Tamiris Beppler Martins ,&nbsp;Joaquim Henrique Lorenzetti Branco ,&nbsp;Taís Beppler Martins ,&nbsp;Gilmar Moraes Santos ,&nbsp;Alexandro Andrade","doi":"10.1016/j.bbih.2024.100941","DOIUrl":"10.1016/j.bbih.2024.100941","url":null,"abstract":"<div><h3>Introduction</h3><div>Investigating the psychological impact caused by the interruption of social interactions on university students during the pandemic is essential, with a view to developing strategies to preserve mental health and academic performance.</div></div><div><h3>Objective</h3><div>To analyze the impact of social isolation during the COVID-19 pandemic on the mental health of university students and propose recommendations for the post-pandemic period.</div></div><div><h3>Method</h3><div>This systematic review was conduced in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and was registered in the International Prospective Register of Systematic Reviews (PROSPERO). Database searches were performed up to December 2024 in PubMed, EMBASE, Web of Science, Scopus, CINAHL, and PsycNET, using the terms “COVID-19,” “social isolation,” “mental health,” and “college students.” Studies were excluded if they focused on non-college populations, other causes of social isolation, physical health, or specific designs.</div></div><div><h3>Results</h3><div>The initial search identified 3051 records and 68 studies were included in this review, with sample off 177,537 university students. Anxiety was the most commonly investigated variable (79.4%), followed by depression (75%) and stress (42.6%). Less frequently, studies highlighted the increase in alcohol and drug consumption and suicidal ideation. Some authors also investigated sleep quality, relating insomnia and emotional changes with the reduction in physical exercise. Anxiety symptoms related to online learning directly impacted academic performance. The assessment of the risk of bias showed that of the 68 studies included, 34 had a low risk of bias, 30 had a moderate risk of bias, and 4 had a high risk of bias.</div></div><div><h3>Conclusion</h3><div>This study highlights the negative impact of the COVID-19 pandemic on the mental health of college students, particularly in relation to symptoms of anxiety, depression, and stress. Post-pandemic interventions should prioritize fostering healthy habits, such as ensuring quality sleep, engaging in moderate physical activity, and raising mental health awareness. Additionally, universities should implement proactive support systems to cultivate a safe and inclusive environment for students.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100941"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026074","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":"Lyme disease associated neurological and musculoskeletal symptoms: A systematic review and meta-analysis","authors":"Ganesh Bushi ,&nbsp;Ashok Kumar Balaraman ,&nbsp;Shilpa Gaidhane ,&nbsp;Suhas Ballal ,&nbsp;Sanjay Kumar ,&nbsp;Mahakshit Bhat ,&nbsp;Shilpa Sharma ,&nbsp;M Ravi Kumar ,&nbsp;Aashna Sinha ,&nbsp;Mahalaqua Nazli Khatib ,&nbsp;Nishant Rai ,&nbsp;Sanjit Sah ,&nbsp;Ambanna Yappalparvi ,&nbsp;Shailesh Kumar Samal ,&nbsp;Doddolla Lingamaiah ,&nbsp;Muhammed Shabil","doi":"10.1016/j.bbih.2024.100931","DOIUrl":"10.1016/j.bbih.2024.100931","url":null,"abstract":"<div><h3>Background and objective</h3><div>Lyme disease, caused by <em>Borrelia burgdorferi</em>, presents major health challenges worldwide, leading to serious neurological and musculoskeletal issues that impact patients' lives and healthcare systems. This systematic review and meta-analysis aim to determine the prevalence and link between Lyme disease and these complications, aiming to enhance clinical and public health approaches.</div></div><div><h3>Methods</h3><div>We systematically searched PubMed, EMBASE, and Web of Science up until April 01, 2024, to find studies reporting the prevalence and severity of neurological and musculoskeletal complications associated with Lyme disease. Screening and data extraction were conducted using Nested Knowledge software. Two independent reviewers performed the quality assessment using the Newcastle-Ottawa Scale. Meta-analyses were performed using R software v4.3, employing a random-effects model.</div></div><div><h3>Results</h3><div>Out of 3576 records, 17 studies were included, involving 3932 participants. These studies revealed significant prevalence of musculoskeletal symptoms (21.1%) and neurological disabilities (18%) among Lyme disease patients. The analysis showed a notable increase in risk for both complications in individuals with Lyme disease, with pooled Risk Ratios (RR) of 1.82 for musculoskeletal symptoms and 1.64 for neurological disabilities, indicating a significantly higher risk compared to control groups. Although heterogeneity across the studies was high, sensitivity analysis confirmed the consistency of our findings. Additionally, there was evidence of publication bias.</div></div><div><h3>Conclusion</h3><div>The study reveals significant neurological and musculoskeletal complications in Lyme disease patients, emphasizing the importance of early diagnosis, comprehensive treatment, and supportive care. The noted heterogeneity and potential publication bias highlight the need for transparent research and further study on long-term outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100931"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048518","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":"Indications for an antidepressive effect of thymosin alpha-1 in a small open-label proof of concept study in common variable immune deficiency patients with depression","authors":"Daniël G. Aynekulu Mersha ,&nbsp;Sarah E. Fromme ,&nbsp;Frank van Boven ,&nbsp;Gara Arteaga-Henríquez ,&nbsp;Annemarie Wijkhuijs ,&nbsp;Marianne van der Ent ,&nbsp;Raf Berghmans ,&nbsp;Bernard T. Baune ,&nbsp;Hemmo A. Drexhage ,&nbsp;Virgil Dalm","doi":"10.1016/j.bbih.2024.100934","DOIUrl":"10.1016/j.bbih.2024.100934","url":null,"abstract":"<div><h3>Background</h3><div>A considerable proportion (21%) of patients with common variable immunodeficiency (CVID) suffers from depression. These subjects are characterized by reduced naïve T cells and a premature T cell senescence similar to that of patients with major depressive disorder (MDD). It is known that T cells are essential for limbic system development/function. Treatment with thymosin α1 (Tα1) is capable to increase the thymus output of naïve T cells.</div></div><div><h3>Objective</h3><div>To treat CVID patients with a comorbid depressive episode with Tα1 to increase naïve T cells and thereby improve mood.</div></div><div><h3>Design</h3><div>A small open-label, proof of concept trial. Five depressed CVID patients (Hamilton Depression Rating Scale, HDRS &gt;12) could be treated with Tα1 (8 weeks, 1.6 mg daily subcutaneously, 1st week, thereafter 1.6 mg twice weekly). At the start, at 8 weeks and 8 weeks after the last injection, the HDRS was recorded and blood samples drawn for measuring naïve and memory T cells, Th17 and Treg cells, hsCRP, IL-6 and IL-7. Outcomes were compared to those of a contrast group (42 MDD patients, same severity but treated as usual (TAU)).</div></div><div><h3>Results</h3><div>In all 5 depressed CVID patients HDRS decreased during Tα1 treatment (with average 52%, TAU decreased scores with 36% in MDD patients). All 5 CVID patients showed an increase in naïve/memory CD4⁺ and CD8⁺ T cell ratios, and in 4 of the 5 patients with detectable IL-6 levels reductions were recorded. TAU did not show such immune improvements. In the 8-week wash-out, depression recurred in the 2 most severe patients, while continued to improve in the others. Immune effects were not sustained in the wash-out.</div></div><div><h3>Conclusion</h3><div>This preliminary small study suggests thymus hormone treatment to have antidepressive and related immune correcting effects. Data urge for larger placebo-controlled trials.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100934"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11762651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048864","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":"Neurological side effects of SARS-CoV-2 vaccination are common and can be severe","authors":"Josef Finsterer","doi":"10.1016/j.bbih.2024.100921","DOIUrl":"10.1016/j.bbih.2024.100921","url":null,"abstract":"","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100921"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932536","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":"Adipose tissue may not be a major player in the inflammatory pathogenesis of Autism Spectrum Disorder","authors":"Baojiang Wang ,&nbsp;Yueyuan Qin ,&nbsp;Yong Chen ,&nbsp;Xiujie Zheng ,&nbsp;Yanjuan Chen ,&nbsp;Juan Zhao ,&nbsp;Feng Zhang ,&nbsp;Shan Duan","doi":"10.1016/j.bbih.2024.100929","DOIUrl":"10.1016/j.bbih.2024.100929","url":null,"abstract":"<div><h3>Purpose</h3><div>Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder increasingly recognized for its strong association with chronic inflammation. Adipose tissue functions as an endocrine organ and can secrete inflammatory cytokines to mediate inflammation. However, its involvement in ASD-related inflammation remains unclear. The present study aimed to clarify the role of adipose tissue in inducing inflammatory responses associated with ASD.</div></div><div><h3>Methods</h3><div>A total of 36 children with ASD and 18 unrelated healthy controls, aged 2–14.5 years, were enrolled in the study. The up-regulated differentially expressed genes from the GSE18123 dataset were subjected to gene ontology (GO) enrichment analysis to explore ASD-associated pathways. Plasma cytokines and adipokines levels were quantified using Milliplex MAP immunoaffinity technology. The BTBR T + Itprtf/J (BTBR) mice that are known for their core ASD behavioral traits and inflammatory phenotypes were employed as an animal ASD model to verify the key clinical findings.</div></div><div><h3>Results</h3><div>GO enrichment analyses revealed immune dysfunction in ASD. Symptom analysis showed that the recruited individuals had typical autistic symptoms. Plasma analysis showed no significant difference in adipokines levels, including adiponectin, leptin, resistin, adipsin, and lipocalin-2, between the ASD and control groups. However, markedly elevated levels of IL-6, IL-8, and tumor necrosis factor (TNF-α) were detected in children with ASD, suggesting that the inflammatory state is independent of adipokines. Similar results were also observed in BTBR autistic mice. Notably, levels of insulin, which are closely related to the exertion of adipokines function, also showed no significant changes.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that inflammation in ASD likely originates from non-adipocyte sources, implying that adipose tissue may not play a major role in inflammatory pathogenesis of ASD. Consequently, targeting adipose-related inflammation may not be an effective treatment approach, providing new directions for the development of targeted interventions.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100929"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985663","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":"Palmitoylethanolamide supplementation for human health: A state-of-the-art systematic review of Randomized Controlled Trials in patient populations","authors":"R. Bortoletto ,&nbsp;C. Comacchio ,&nbsp;M. Garzitto ,&nbsp;F. Piscitelli ,&nbsp;M. Balestrieri ,&nbsp;M. Colizzi","doi":"10.1016/j.bbih.2024.100927","DOIUrl":"10.1016/j.bbih.2024.100927","url":null,"abstract":"<div><div>Interest in preventative dietary interventions for human health has increasingly focused on the endocannabinoid (eCB)-like compound palmitoylethanolamide (PEA), a bioactive lipid mediator with anti-inflammatory, analgesic, and neuroprotective properties. This Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020-compliant systematic review aimed at collecting and comprehensively discussing all available data from Randomized Controlled Trials (RCTs) evaluating the efficacy and tolerability of PEA supplementation across human illnesses in patient populations. Overall, 48 eligible outputs from 47 RCTs were extracted, covering neuropsychiatric (<em>n</em> = 15), neurological (<em>n</em> = 17), somatic (<em>n</em> = 13), and visceral (<em>n</em> = 11) disturbances, as well as PEA effects on blood/plasma or other tissue biomarkers (<em>n</em> = 10). The strongest evidence emerged from RCTs exploring PEA impact on pain management and measures of general wellbeing, especially in its ultramicronized/micronized or cold-water dispersible formulations, showing good tolerability compared to controls. Also, alongside symptom improvement, PEA demonstrated to modulate biomarkers early altered in the initial phases of an illness or contributing to its progression, suggesting a disease-modifying potential. This systematic review provided a comprehensive overview of the therapeutic potential of PEA across RCTs, highlighting its versatility either as monotherapy or add-on treatment for various clinical conditions.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100927"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017368","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":"What is the relationship between exposure to environmental pollutants and severe mental disorders? A systematic review on shared biological pathways","authors":"Pierluigi Catapano,&nbsp;Mario Luciano,&nbsp;Salvatore Cipolla,&nbsp;Daniela D'Amico,&nbsp;Alessandra Cirino,&nbsp;Maria Chiara Della Corte,&nbsp;Gaia Sampogna,&nbsp;Andrea Fiorillo","doi":"10.1016/j.bbih.2024.100922","DOIUrl":"10.1016/j.bbih.2024.100922","url":null,"abstract":"<div><div>Severe mental disorders are multi-dimensional constructs, resulting from the interaction of genetic, biological, psychosocial, and environmental factors. Among the latter, pollution and climate change are frequently being considered in the etiopathogenesis of severe mental disorders. This systematic review aims to investigate the biological mechanisms behind the relationship between environmental pollutants, climate change, and mental disorders. An extensive literature search was performed on PubMed, Scopus, and APA PsycInfo databases according to the PRISMA guidelines. Articles were considered eligible if they involved humans or animals examining the association between exposure to environmental pollutants and if the resulting biological mechanisms that may have an impact on mental health and may support or even cause severe mental disorders (SMD) are assessed. For this reason, only studies dealing with biomarkers or biological pathways were taken into account. The 47 papers included in the review were divided into two groups: those conducted on human participants (15 studies) and those utilizing animal models (31 studies); one study included both humans and animals. Studies carried out with humans, which are mainly focused on measuring the impact of particulate matter (PM_2.5 and PM₁₀) exposure on mental health, showed an increased risk of depression or psychotic relapses through the inflammation and oxidative stress pathways, or through the alteration of the hypothalamic-pituitary-adrenal (HPA) axis. Animal models showed the potential impact of pollution on brain functioning through increased inflammatory responses, oxidative stress, HPA axis disruption, hippocampal damage, and neurotransmitters dysregulation. Our findings show that environmental pollutants have an impact on human mental health through different biological pathways. The biological mechanisms by which environmental pollution and climate change influence the onset and exacerbation of severe mental disorders are complex and include gene expression, inflammation, oxidative stress, and anatomical brain changes. A better understanding of those pathways is important for the progress of knowledge on the pathophysiology of severe mental disorders according to the one health model, that promotes a collaborative, multisectoral, and transdisciplinary approach across various levels to optimize health outcomes by recognizing the interconnectedness of humans, animals, plants, and their shared environment.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100922"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11719278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973697","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":"Should we consider microbiota-based interventions as a novel therapeutic strategy for schizophrenia? A systematic review and meta-analysis","authors":"Lucas Hassib ,&nbsp;Alexandre Kanashiro ,&nbsp;João Francisco Cordeiro Pedrazzi ,&nbsp;Bárbara Ferreira Vercesi ,&nbsp;Sayuri Higa ,&nbsp;Íris Arruda ,&nbsp;Yago Soares ,&nbsp;Adriana de Jesus de Souza ,&nbsp;Alceu Afonso Jordão ,&nbsp;Francisco Silveira Guimarães ,&nbsp;Frederico Rogério Ferreira","doi":"10.1016/j.bbih.2024.100923","DOIUrl":"10.1016/j.bbih.2024.100923","url":null,"abstract":"<div><div>Schizophrenia is a chronic psychiatric disorder characterized by a variety of symptoms broadly categorized into positive, negative, and cognitive domains. Its etiology is multifactorial, involving a complex interplay of genetic, neurobiological, and environmental factors, and its neurobiology is associated with abnormalities in different neurotransmitter systems. Due to this multifactorial etiology and neurobiology, leading to a wide heterogeneity of symptoms and clinical presentations, current antipsychotic treatments face challenges, underscoring the need for novel therapeutic approaches. Recent studies have revealed differences in the gut microbiome of individuals with schizophrenia compared to healthy controls, establishing an intricate link between this disorder and gastrointestinal health, and suggesting that microbiota-targeted interventions could help alleviate clinical symptoms. Therefore, this meta-analysis investigates whether gut microbiota manipulation can ameliorate psychotic outcomes in patients with schizophrenia receiving pharmacological treatment. Nine studies (n = 417 participants) were selected from 81 records, comprising seven randomized controlled trials and two open-label studies, all with a low risk of bias, included in this systematic review and meta-analysis. The overall combined effect size indicated significant symptom improvement following microbiota treatment (Hedges' g = 0.48, 95% CI = 0.09 to 0.88, p = 0.004, I² = 62.35%). However, according to Hedges' g criteria, the effect size was small (approaching moderate), and study heterogeneity was moderate based on I² criteria. This review also discusses clinical and preclinical studies to elucidate the neural, immune, and metabolic pathways by which microbiota manipulation, particularly with <em>Lactobacillus</em> and <em>Bifidobacterium</em> genera, may exert beneficial effects on schizophrenia symptoms via the gut-brain axis. Finally, we address the main confounding factors identified in our systematic review, highlight key limitations, and offer recommendations to guide future high-quality trials with larger participant cohorts to explore microbiome-based therapies as a primary or adjunctive treatment for schizophrenia.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100923"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017373","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":"Structural and functional brain correlates of the neutrophil- and monocyte-to-lymphocyte ratio in neuropsychiatric disorders","authors":"Roger McIntosh","doi":"10.1016/j.bbih.2024.100940","DOIUrl":"10.1016/j.bbih.2024.100940","url":null,"abstract":"<div><div>Skews in the neutrophil-to-lymphocyte ratio (NLR) and monocyte-to-lymphocyte ratio (MLR) increasingly demonstrate prognostic capability in a range of acute and chronic mental health conditions. There has been a recent uptick in structural and functional magnetic responance imaging data corroborating the role of NLR and MLR in a cluster of neuropsychiatric disorders that are characterized by cognitive, affective, and psychomotor dysfunction. Moreover, these deficits are mostly evident in setting of acute and chronic disease comorbidity implicating aging and immunosenescent processes in the manifestation of these geriatric syndromes. The studies reviewed in this special edition implicate neutrophil and monocyte expansion relative to lymphocytopenia in the sequelae of depression, cognitive and functional decline, as well as provide support from a range of neuroimaging techniques that identify brain alteartions concommitant with expansion of the NLR or MLR and the sequelae of depression, dementia, and functional decline.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100940"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061077","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":"Exploring the role of inflammatory biomarkers in trigeminal neuralgia","authors":"Shenglong Lai,&nbsp;Haiyang Li,&nbsp;Yazhou Xing,&nbsp;Du Wu,&nbsp;Lin Wang,&nbsp;Qinghua Liang","doi":"10.1016/j.bbih.2024.100930","DOIUrl":"10.1016/j.bbih.2024.100930","url":null,"abstract":"<div><h3>Background</h3><div>Trigeminal neuralgia (TN) is a severe facial pain disorder with complex etiology. Inflammation has been suggested as a contributing factor to TN pathogenesis. This study investigates the causal relationship between inflammatory biomarkers, including 41 circulating inflammatory cytokines, C-reactive protein (CRP), and procalcitonin (PCT), and TN using Mendelian randomization (MR) analysis.</div></div><div><h3>Methods</h3><div>A two-sample MR approach was employed using genome-wide association study (GWAS) data from 8293 Finnish individuals for inflammatory cytokines and data from the FinnGen database for TN. Instrumental variables (IVs) were selected based on genome-wide significance and clumping thresholds to avoid linkage disequilibrium. Inverse variance weighting (IVW) was used as the primary method, complemented by MR Egger regression, weighted median, simple mode, and weighted mode methods. Additionally, Bayesian Weighted MR (BWMR) and Multivariable MR (MVMR) were utilized to validate the findings and explore potential confounders.</div></div><div><h3>Results</h3><div>The present MR analysis identified significant causal associations for three inflammatory cytokines with TN. Stem cell growth factor beta (SCGF-β) (OR = 1.362, 95% CI = 1.049–1.770, p = 0.021) and Interleukin-4 (IL-4) (OR = 1.533, 95% CI = 1.014–2.316, p = 0.043) were positively associated with TN, while Interleukin-16 (IL-16) (OR = 0.720, 95% CI = 0.563–0.921, p = 0.009) had a protective effect. CRP levels were also linked to TN risk (OR = 0.751, 95% CI = 0.593–0.951, p = 0.017). No significant causal effect of PCT on TN was observed. Sensitivity analyses confirmed the robustness of these findings, showing no evidence of horizontal pleiotropy or heterogeneity.</div></div><div><h3>Conclusion</h3><div>This study highlights specific inflammatory biomarkers that may play pivotal roles in TN pathogenesis. SCGF-β and IL-4 are potential therapeutic targets due to their facilitative effects on TN, while IL-16 could offer protective benefits. CRP's association with TN further supports the involvement of systemic inflammation in this condition. These findings provide novel insights into TN's inflammatory mechanisms, suggesting new avenues for targeted interventions.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100930"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11743902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017337","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}