Brain, behavior, & immunity - health最新文献

{"title":"Mental distress and inflammation in bladder cancer: The nerve makes things less vague","authors":"Iveta Mikolaskova ,&nbsp;Yori Gidron ,&nbsp;Vladimira Durmanova ,&nbsp;Magda Suchankova ,&nbsp;Maria Bucova ,&nbsp;Luba Hunakova","doi":"10.1016/j.bbih.2025.100995","DOIUrl":"10.1016/j.bbih.2025.100995","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to explore the interaction between perceived stress, life satisfaction, heart rate variability (HRV), and immune-inflammatory markers in bladder cancer patients. We investigated how HRV moderates the relationship between psychological distress and levels of TNF-α and TGF-β cytokines. We hypothesized that high vagal nerve activity, as indicated by higher HRV, mitigates the impact of perceived stress and life dissatisfaction on inflammation.</div></div><div><h3>Methods</h3><div>The study included 73 patients with bladder cancer. HRV was determined from a 5-min ECG recording, focusing on the standard deviation of normal-to-normal interbeat intervals (SDNN). Psychological distress was measured using the Perceived Stress Scale (PSS), and life satisfaction was evaluated with the Life Satisfaction Questionnaire (LSQ). Serum concentrations of TNF-α and plasma levels of TGF-β were determined using sandwich ELISA.</div></div><div><h3>Results</h3><div>We found evidence that HRV modulates the relation between perceived stress and inflammation. In patients with low HRV (SDNN &lt;20 ms), PSS was positively correlated with serum level of TNF-α and negatively with the level of TGF-β, while life satisfaction was positively correlated with TGF-β. These relationships were not significant in patients with high HRV (SDNN ≥20 ms).</div></div><div><h3>Conclusion</h3><div>Our findings suggest that high vagal activity, as indicated by higher HRV, may mitigate the adverse effects of psychological distress on immune-inflammatory responses in patients with bladder cancer. Stress-related inflammation took place under conditions of low HRV, highlighting the potential role of autonomic regulation in cancer prognosis. Future research should further explore these relationships to develop interventions aimed at improving patient outcomes through stress management and enhanced vagal nerve activity to regulate inflammation in cancer.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"46 ","pages":"Article 100995"},"PeriodicalIF":3.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874852","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":"Social relationships and immune aging in early midlife: Evidence from the National Longitudinal Study of Adolescent to Adult Health","authors":"Farizah I. Rob ,&nbsp;Rebecca C. Stebbins ,&nbsp;Jennifer Momkus ,&nbsp;Chantel L. Martin ,&nbsp;Kathleen Mullan Harris ,&nbsp;Allison E. Aiello","doi":"10.1016/j.bbih.2025.100993","DOIUrl":"10.1016/j.bbih.2025.100993","url":null,"abstract":"<div><div>Aging of the immune system is characterized by changes in the T-cell compartment, including a decrease in naïve T-cells and an increase in memory T-cells. Stress exposures are known to predict accelerated immune aging in older adults. However, social relationships, which are often linked to stress mechanisms, have not been widely studied in relation to these adaptive immune biomarkers, particularly in younger populations. We examined associations between social relationships, in terms of quantity (Social Network Index, Close Contacts Index) and quality of relationships (spouse/partner, friends, and family members), and immune aging in a U.S-representative early midlife population (age 33–44) from Wave V of the National Longitudinal Study of Adolescent to Adult Health (n = 4451). DNA methylation data of venous blood samples collected during Wave V were used to compute CD4⁺ memory:naïve, CD8⁺ memory:naïve, and total CD8+:CD4+ T cell ratios; higher values indicate a more aged immune profile. Results from survey-weighted linear regression models adjusted for age, sex, race/ethnicity, and education indicated higher number of close friends and frequency of contact, alongside higher quality relationships with family members were associated with decreases in CD4⁺ memory:naive ratios. The results for CD8⁺ memory:naïve and CD8+:CD4+ ratios were mostly non-significant. Our findings suggest that higher quantity and quality of social relationships may help protect against immune aging, particularly in the CD4⁺ T cell compartment, prior to midlife. This underscores the importance of interventions that enhance social relationships throughout life to promote healthy longevity.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100993"},"PeriodicalIF":3.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843281","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":"Depressive symptoms partially mediate the relationship between psychosocial factors and epigenetic age acceleration in a multi-racial/ethnic sample of older adults","authors":"Lauren A. Opsasnick ,&nbsp;Wei Zhao ,&nbsp;Lauren L. Schmitz ,&nbsp;Scott M. Ratliff ,&nbsp;Jessica D. Faul ,&nbsp;Xiang Zhou ,&nbsp;Belinda L. Needham ,&nbsp;Jennifer A. Smith","doi":"10.1016/j.bbih.2025.100994","DOIUrl":"10.1016/j.bbih.2025.100994","url":null,"abstract":"<div><div>Psychosocial factors, including cumulative psychosocial stress and loneliness, have been linked to epigenetic aging in older adults. Further, depressive symptoms have established relationships with both psychosocial factors and epigenetic aging. However, it is not known whether depressive symptoms mediate the association between psychosocial factors and epigenetic aging.</div><div>We conducted linear regression models to examine associations between psychosocial stress, loneliness, and depressive symptoms and five epigenetic age acceleration (AA) measures estimated by DNA methylation in a multi-racial/ethnic sample of 2681 older adults from the Health and Retirement Study (mean age: 70.4 years). For all identified associations, we tested for effect modification by sex and educational attainment and performed mediation analysis to characterize the role of depressive symptoms on these associations.</div><div>Psychosocial stress, loneliness, and depressive symptoms were each associated with at least one measure of epigenetic AA (FDR q &lt; 0.05). Further, we observed interactions between loneliness, psychosocial stress, and sex on DunedinPACE, as well as loneliness and educational attainment on GrimAA, PhenoAA, and DunedinPACE, with females and individuals without a college degree appearing more sensitive to the psychosocial effects on epigenetic aging. Depressive symptoms mediated between 24 % and 35 % of the relationships between psychosocial stress and HannumAA, GrimAA, and DunedinPACE, as well as 40 % and 37 % of the relationships between loneliness and both GrimAA and DunedinPACE, respectively.</div></div><div><h3>Results</h3><div>from this study may help elucidate the relationship between psychosocial factors and epigenetic aging, which is critical in understanding the biological mechanisms through which psychosocial factors may contribute to age-related disease.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100994"},"PeriodicalIF":3.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834919","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":"HIV and Low Omega-3 Levels May Heighten Hippocampal Volume Differences Between Men and Women With Substance Use","authors":"Hong Lai ,&nbsp;Jiachen Zhuo ,&nbsp;Glenn Treisman ,&nbsp;Gary Gerstenblith ,&nbsp;David D. Celentano ,&nbsp;Yihong Yang ,&nbsp;Betty Jo Salmeron ,&nbsp;Hong Gu ,&nbsp;Thorsten M. Leucker ,&nbsp;Xiao Liang ,&nbsp;Raul N. Mandler ,&nbsp;Jag Khalsa ,&nbsp;Óscar Peña-Nogales ,&nbsp;Shaoguang Chen ,&nbsp;Shenghan Lai ,&nbsp;Elana Rosenthal ,&nbsp;Karl Goodkin ,&nbsp;Vincent A. Magnotta","doi":"10.1016/j.bbih.2025.100988","DOIUrl":"10.1016/j.bbih.2025.100988","url":null,"abstract":"<div><h3>Background</h3><div>Sex differences in hippocampal volumes are well-documented, but their interaction with HIV status and omega-3 fatty acids—particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—remains unclear, especially in underserved populations. This study examines how HIV and omega-3 fatty acids influence sex differences in hippocampal volume and explores whether cognitive performance related to episodic memory modifies the association of omega-3 levels with hippocampal volume, considering both HIV status and sex.</div></div><div><h3>Methods</h3><div>We enrolled 166 participants aged over 45 years from a Baltimore, Maryland cohort. Brain MRIs were performed using a 3.0-T Siemens scanner, and volumetric segmentation was conducted with FreeSurfer (version 6.0), adjusting for intracranial volume (ICV).</div></div><div><h3>Results</h3><div>Our study found that: (1) Among HIV-negative participants, females had significantly lower hippocampal volumes than males in 1 of 26 regions, whereas HIV-positive females had lower volumes in 13 of 26 regions (p &lt; 0.006 for HIV-negative vs. HIV-positive females), (2) In HIV-positive individuals with EPA levels ≤0.40 %, females exhibited lower volumes in 11 of 26 regions, compared to no differences in those with EPA levels &gt;0.40 % (p = 0.0003 for ≤0.40 % vs. &gt;0.40 %), (3) Across all participants, lower EPA and DHA levels were associated with greater sex differences in hippocampal volumes, which diminished or disappeared at higher EPA and DHA levels (p &lt; 0.00001 for EPA ≤0.40 % vs. &gt;0.40 %; p = 0.004 for DHA ≤2.0 % vs. &gt;2.0 %), and (4) Among Adults with lower episodic memory, higher log-scaled EPA levels were independently associated with greater hippocampal volume.</div></div><div><h3>Conclusions</h3><div>HIV may amplify sex differences in hippocampal volumes, disproportionately affecting females. Higher EPA and DHA levels may mitigate these effects, suggesting a protective role against hippocampal atrophy. Further studies are warranted to confirm these findings and explore whether the benefits extend to males with HIV or individuals without HIV.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100988"},"PeriodicalIF":3.7,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799193","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":"Cardiovascular health and its association with dementia, Parkinson's Disease, and mortality among UK older adults","authors":"Michael F. Georgescu ,&nbsp;May A. Beydoun ,&nbsp;Jordan Weiss ,&nbsp;Jagdish Kubchandani ,&nbsp;Sri Banerjee ,&nbsp;Alyssa A. Gamaldo ,&nbsp;Michele K. Evans ,&nbsp;Alan B. Zonderman","doi":"10.1016/j.bbih.2025.100986","DOIUrl":"10.1016/j.bbih.2025.100986","url":null,"abstract":"<div><h3>Background</h3><div>Previous research has primarily examined individual factors of cardiovascular health (CVH) and disease in PD and dementia, but no study has examined CVH measures with PD, dementia, and mortality simultaneously while accounting for potentially confounding factors.</div></div><div><h3>Objectives</h3><div>To examine the relationship between CVH, all-cause dementia, Parkinson's disease (PD), and mortality, focusing on associations and health transitions from a large population-based study.</div></div><div><h3>Methods</h3><div>We investigated these relationships using Cox Proportional Hazards and multistate parametric models with Weibull regression from the UK Biobank data (n = 269,816, Age = 50 + y individuals, ≤15y follow-up, 2006–2021).</div></div><div><h3>Results</h3><div>Full Cox models found poor CVH (measured with standardized reverse-coded Life's Essential 8 total score, LE8_zrev), to be associated with increased risks for all-cause dementia (Hazard Ratio (HR) = 1.14, 95 % CI: 1.11–1.18, P &lt; 0.001) and all-cause mortality (HR = 1.31, 95 % CI: 1.29–1.33, P &lt; 0.001). Unlike “Healthy to PD” and “Dementia→Death” transitions, PD→Death (Weibull full model: HR = 1.18, 95 % CI: 1.06–1.31, P = 0.002), Healthy→dementia (HR = 1.15, 95 % CI: 1.12–1.19, P &lt; 0.001), and Healthy→Death (HR = 1.33, 95 % CI: 1.32–1.35, P &lt; 0.001) exhibited a positive relationship with poor CVH.</div></div><div><h3>Conclusions</h3><div>Poor CVH is directly associated with an increased risk of mortality from PD, transition into Dementia, and all-cause mortality without dementia or PD occurrence. Clinicians should aggressively screen for and manage CVH risk measures to reduce the risk of poor cognitive health outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100986"},"PeriodicalIF":3.7,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143747663","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":"Smoking disrupts the relationship between cerebrospinal fluid IL-1β and multiple subdimensions of sleep","authors":"Yueling Hu ,&nbsp;Siyuan Li ,&nbsp;Yingjie Chen ,&nbsp;Xingguang Luo ,&nbsp;Yu-Hsin Chen ,&nbsp;Yimin Kang ,&nbsp;Weiming Hu ,&nbsp;Li Chen ,&nbsp;Siling Ye ,&nbsp;Xinchen Zhou ,&nbsp;Yanlong Liu ,&nbsp;Fan Wang ,&nbsp;Yuying Li","doi":"10.1016/j.bbih.2025.100987","DOIUrl":"10.1016/j.bbih.2025.100987","url":null,"abstract":"<div><h3>Objective</h3><div>Inflammatory factors and cigarette smoking have been associated with sleep disorders but molecular mechanisms that regulate sleep, specifically the role of interleukin-1β (IL-1β), remain controversial. Individuals’ cerebrospinal fluid (CSF) IL-1β, smoking behavior, and sleep data were collected to investigate how smoking may influence the relationship between CSF IL-1β and sleep via moderation analysis.</div></div><div><h3>Methods</h3><div>A total of 191 Chinese male patients, including 104 non-smokers and 87 active smokers, scheduled for anterior cruciate ligament reconstructive surgery, were recruited. Pittsburgh Sleep Quality Index (PSQI) scores were collected prior to surgery, and CSF samples were obtained during preoperative lumbar puncture.</div></div><div><h3>Results</h3><div>Active smokers compared to non-smokers exhibited higher scores across various subdimensions of PSQI, specifically poorer sleep quality, increased sleep latency, reduced sleep efficiency, and heightened sleep disturbance (all p &lt; 0.05). Positive correlations were observed between CSF IL-1β levels and PSQI total scores, as well as several subdimensions of sleep (all p &lt; 0.05) in non-smokers. In contrast, a negative correlation was observed between CSF IL-1β levels and sleep efficiency scores (p &lt; 0.05) among active smokers. Moderation analysis revealed that smoking negatively moderated the relationship between CSF IL-1β and sleep, particularly in PSQI total scores (β = −0.95, p &lt; 0.001), sleep latency scores (β = −1.05, p &lt; 0.001), and sleep disturbance scores (β = −0.45, p &lt; 0.05).</div></div><div><h3>Conclusions</h3><div>The current study found that smoking disrupts multiple subdimensions of sleep and moderates the effect of the neuroinflammatory factor CSF IL-1β on PSQI sleep latency and sleep disturbance scores.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100987"},"PeriodicalIF":3.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143760773","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":"SARS-CoV-2-induced sensory perturbations: A narrative review of clinical phenotypes, molecular pathologies, and possible interventions","authors":"Randal A. Serafini ,&nbsp;Justin J. Frere ,&nbsp;Ilinca M. Giosan ,&nbsp;Chinwe A. Nwaneshiudu","doi":"10.1016/j.bbih.2025.100983","DOIUrl":"10.1016/j.bbih.2025.100983","url":null,"abstract":"<div><h3>Background</h3><div>The acute and post-acute sequelae of SARS-CoV-2 infection have been of great clinical interest since the inception of the COVID-19 pandemic. Despite a high prevalence of individuals with persistent symptoms, a wholistic view of the effects of SARS-CoV-2 on special sensory systems is lacking. Considering the significant impact of normal sensory function on quality of life, the goal of this review is to highlight unresolved issues related to SARS-CoV-2-associated insults to the sensory nervous system.</div></div><div><h3>Major findings</h3><div>In this narrative review, we discuss the epidemiology of SARS-CoV-2-induced sensory perturbations, underlying pathological mechanisms, and possible therapeutic strategies across the olfactory, gustatory, somatosensory, visual, and auditory systems. Examined literature included studies with human biospecimens, human-derived cell lines, and naturally susceptible animal models, which highlighted evidence of persistent functional disruption in all sensory systems. SARS-CoV-2 infection was associated with persistent inflammation in the olfactory epithelium/bulb, somatosensory ganglia, and gustatory systems, long-term transcriptional perturbations in the sensory central nervous system and peripheral nervous system, and detectable degeneration/apoptosis in the gustatory and visual systems. Few studies have proposed evidence-based therapeutic strategies for attenuating specific sensory abnormalities after SARS-CoV-2 infection.</div></div><div><h3>Conclusion</h3><div>While the olfactory system, and to some extent the visual and somatosensory systems, have been more thoroughly investigated from symptomatology, behavioral and molecular perspectives, there is still an unmet need for the development of therapeutics to treat COVID-induced impairment of these systems. Further, additional attention must be placed on COVID-associated impairment of the gustatory, visual, and auditory systems, which lack detailed mechanistic investigations into their pathogenesis.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100983"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143724314","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":"Temporal dynamics of inflammatory, platelet, and neurotrophic markers during social stress in relation to suicidal ideation and suicide attempt history","authors":"Aiste Lengvenyte ,&nbsp;Emilie Olié ,&nbsp;Fabrice Cognasse ,&nbsp;Hind Hamzeh-Cognassse ,&nbsp;Adrian Alacreu-Crespo ,&nbsp;Philippe Courtet","doi":"10.1016/j.bbih.2025.100984","DOIUrl":"10.1016/j.bbih.2025.100984","url":null,"abstract":"<div><div>Interpersonal stress is a major precipitant of suicidal ideation (SI) and suicide attempts (SA), yet the underlying biological mechanisms remain unclear. This study examined dynamic plasma concentrations of inflammatory, platelet activation, and neurotrophic markers during acute social stress in 76 depressed women (mean age: 39.7 ± 1.39 years) with and without SA history or recent SI. Participants underwent the Trier Social Stress Test, with biomarkers measured at five time points before, during, and after the stressor. Covariate-adjusted growth curve models and area under the curve analyses were applied. SI was associated with elevated overall TNF-α levels (0.82 ± 0.05 vs. 0.61 ± 0.05, p = 0.039). Participants without SI showed cubic trajectories in TNF-α (t₂₂₈ = 4.76, p &lt; 0.001) and MIP-1β (t₂₃₅ = 2.12, p = 0.035), and quadratic trajectories in platelet markers TSP-1 (t₂₇₄ = −2.42, p = 0.016), PF-4 (t₂₇₄ = −2.25, p = 0.025), and NAP-2 (t₂₇₄ = −2.43, p = 0.016), which were absent in participants with SI. Cubic patters in inflammatory responses were also observed in participants without SA history, but not in suicide attempters (TNF-α: t₂₂₈ = 3.15, p = 0.030; MIP-1β: t₂₃₅ = 2.74, p = 0.007). Meanwhile, participants with SI or SA, but not those without, showed a linear BDNF increase (t₂₇₅ = 2.39, p = 0.017; t₂₇₅ = 2.28, p = 0.024, respectively). These findings suggest that SI and SA may be associated with impaired dynamic immune-inflammatory, platelet, and neurotrophic systems responses to acute interpersonal stress, reflecting systemic biological rigidity.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100984"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143695921","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":"Predictors of fatigue progression in long COVID among young people","authors":"Elias Myrstad Brodwall ,&nbsp;Joel Selvakumar ,&nbsp;Lise Beier Havdal ,&nbsp;Silke Sommen ,&nbsp;Lise Lund Berven ,&nbsp;Erin Cvejic ,&nbsp;Vegard Bruun Bratholm Wyller ,&nbsp;Maria Pedersen","doi":"10.1016/j.bbih.2025.100982","DOIUrl":"10.1016/j.bbih.2025.100982","url":null,"abstract":"<div><div>Long COVID, or post-COVID-19 condition (PCC), has emerged as a significant health concern, with fatigue being the most prevalent persistent symptom among young people. However, research on predictors of fatigue progression in young populations is limited. This study aimed to investigate factors during acute SARS-CoV-2 infection that could predict fatigue progression between six and 12 months post-infection in a cohort of young people with chronic fatigue following COVID-19. Data from the Long-Term Effects of COVID-19 in Adolescents (LoTECA) project were analyzed. A total of 93 participants (mean age 18.5 years, 84 % female) with chronic fatigue at six months, completed the 12-month follow-up. Multivariate analyses identified non-European ethnicity, higher interferon gamma (IFN-γ) levels, and lower RR-interval (higher resting heart rate) during acute infection as significant predictors of fatigue progression from six to 12 months. These three factors explained 21 % of the variance in the fatigue score, highlighting the importance of ethnicity, immune response, and autonomic function in the trajectory of long COVID fatigue. Early identification and targeted interventions, particularly for ethnic minorities and those with specific immune or autonomic markers during acute infection, may be helpful in reducing long-term fatigue. Further research is needed to explore treatment strategies for affected young populations.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100982"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697250","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":"A case of MOGAD with rectal adenocarcinoma: Comorbidity or paraneoplastic neurological syndrome?","authors":"Yiyi Luo ,&nbsp;Gang Peng ,&nbsp;Jiahua Liang ,&nbsp;Xuwei Song ,&nbsp;Jiayu Tang","doi":"10.1016/j.bbih.2025.100985","DOIUrl":"10.1016/j.bbih.2025.100985","url":null,"abstract":"<div><h3>Background</h3><div>Myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare autoimmune disease characterized primarily by central nervous system demyelination. We report a rare case of MOGAD coexisting with rectal adenocarcinoma.</div></div><div><h3>Case report</h3><div>A 59-year-old female presented with fever and bilateral lower limb weakness. MRI of the brain revealed abnormal signals in multiple regions of the cerebrum, brainstem, and spinal cord. Both serum and cerebrospinal fluid tested positive for MOG antibodies. The symptoms improved after steroid therapy. During hospitalization, colonoscopy and pathological examination revealed rectal cancer, which was subsequently treated surgically. After six months of follow-up, neither the tumor nor MOGAD recurred.</div></div><div><h3>Conclusion</h3><div>Paraneoplastic etiologies may also contribute to the development of MOGAD. To date, no cases of MOGAD associated with rectal cancer have been reported. It remains uncertain whether paraneoplastic neurologic syndrome (PNS) is involved in this patient.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100985"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143724315","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}