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Sex differences in the mediating role of brain-derived neurotrophic factor between inflammation and memory in cirrhotic patients with minimal hepatic encephalopathy 脑源性神经营养因子在肝硬化伴轻度肝性脑病患者炎症和记忆之间中介作用的性别差异
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-22 DOI: 10.1016/j.bbih.2025.100998
Daniela Batallas , Juan José Gallego , Franc Casanova-Ferrer , Adriá López-Gramaje , Pablo Rivas-Diaz , Javier Megías , Desamparados Escudero-García , Lucía Durbán , Salvador Benlloch , Amparo Urios , Vanesa Hidalgo , Alicia Salvador , Carmina Montoliu
Minimal hepatic encephalopathy (MHE) affects attention, visuo-motor coordination, and visual perception, with mixed evidence on its impact on memory. Brain-derived neurotrophic factor (BDNF) is associated with memory dysfunction, and plays a crucial role in modulating neuroplasticity. This study investigates the mediating role of BDNF in the relationship between pro-inflammatory cytokines (IL-6, IL-15, IL-18), and declarative memory performance, and the moderating effects of sex. Sixty-eight cirrhotic patients and 22 healthy volunteers performed the Psychometric Hepatic Encephalopathy Score for MHE diagnosis and logical memory subtest (Wechsler Memory Scale-III). Moderated mediation analysis using bias-corrected bootstrapping and multiple regression was performed. Results showed that increased levels of IL-18 and IL-15 were significantly associated with lower BDNF levels (p = 0.03 and p = 0.02 respectively). However, no direct effect was observed between IL-18 and IL-15 and memory. The conditional effects of BDNF on memory were significant only for women with and without MHE, and lower BDNF levels were associated with lower memory performance (without MHE: p = 0.002; MHE: p = 0.001). Moreover, BDNF mediated indirectly the relationship between pro-inflammatory cytokines and memory. IL-18 and IL-15 impacted memory through reduced BDNF levels only in women with and without MHE, whereas IL-6 showed no significant effect on BDNF or memory across groups. These findings underscore the important role of BDNF in memory in cirrhotic patients, especially women with MHE, by mediating the IL-18 and IL-15 effects. The study highlights the role of IL-18 and IL-15 cytokines in neuroplasticity-related memory decline, positioning BDNF as a key biomarker for inflammation-associated cognitive impairment in this population.
轻度肝性脑病(MHE)影响注意力、视觉运动协调和视觉感知,其对记忆的影响证据不一。脑源性神经营养因子(BDNF)与记忆功能障碍有关,在调节神经可塑性中起着至关重要的作用。本研究探讨了BDNF在促炎细胞因子(IL-6, IL-15, IL-18)和陈述性记忆表现之间的中介作用,以及性别的调节作用。68名肝硬化患者和22名健康志愿者进行了MHE诊断的肝性脑病心理测量评分和逻辑记忆亚测试(韦氏记忆量表- iii)。使用偏差校正引导和多元回归进行了有调节的中介分析。结果显示,IL-18和IL-15水平升高与BDNF水平降低显著相关(p = 0.03和p = 0.02)。然而,IL-18和IL-15对记忆没有直接影响。BDNF对记忆的条件效应仅在有和没有MHE的女性中显着,较低的BDNF水平与较低的记忆表现相关(没有MHE: p = 0.002;MHE: p = 0.001)。此外,BDNF间接介导了促炎细胞因子与记忆之间的关系。IL-18和IL-15仅在有和没有MHE的女性中通过降低BDNF水平影响记忆,而IL-6在各组中对BDNF或记忆没有显著影响。这些发现强调了BDNF通过介导IL-18和IL-15的作用在肝硬化患者,特别是MHE患者的记忆中的重要作用。该研究强调了IL-18和IL-15细胞因子在神经可塑性相关的记忆衰退中的作用,将BDNF定位为该人群中炎症相关认知障碍的关键生物标志物。
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引用次数: 0
Salivary lactoferrin levels in Down Syndrome: a case-control study 唐氏综合症患者唾液乳铁蛋白水平:一项病例对照研究
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-21 DOI: 10.1016/j.bbih.2025.100999
Desireé Antequera , Lucía Sande , Eliane García Mato , Deborah Romualdi , Laura Carrero , Cristina Municio , Pedro Diz , Eva Carro
Individuals with Down Syndrome (DS) have a high age-dependent risk of developing Alzheimer's disease (AD). In addition to genetic causes, this high risk involves dysregulated immune-inflammatory system. Low lactoferrin levels, one of the main antimicrobial proteins present in saliva, has been associated with AD. Here, we evaluated whether salivary lactoferrin levels change across the life span of individuals with DS. The study included 152 participants, 72 subjects with DS and 80 euploid individuals, and were divided into those under and over 45 years of age, accordingly with the age-dependent risk of AD. Median of salivary lactoferrin were higher among DS individual, in parallel to salivary total protein, but there were no differences in the ratio of lactoferrin to total protein in saliva between groups. Only DS individuals had higher median salivary lactoferrin levels in the age group under 45 years. Meanwhile non-significant differences were detected for the ratio salivary lactoferrin levels to total salivary protein between groups under 45 years, those levels were lower in DS subjects over 45 years old compared with the age-matched control group. Furthermore, the ratio of salivary lactoferrin levels to total protein in DS was associated with cognitive decline being lower in demented groups compared with mild and moderate cognitive impairment groups. In summary, this study indicates that salivary lactoferrin was dysregulated in DS, with significant lower ratio of salivary lactoferrin levels to total salivary proteins in individuals with DS over 45 years old, a population with a gradually increasing risk of AD.
患有唐氏综合症(DS)的个体患阿尔茨海默病(AD)的年龄依赖性风险很高。除了遗传原因外,这种高风险还涉及免疫炎症系统失调。低乳铁蛋白水平,存在于唾液中的主要抗菌蛋白之一,与AD有关。在这里,我们评估了唾液乳铁蛋白水平是否在DS患者的整个生命周期中发生变化。该研究包括152名参与者,72名DS患者和80名整倍体个体,并根据AD的年龄依赖性风险分为45岁以下和45岁以上人群。DS个体唾液乳铁蛋白中位数较高,与唾液总蛋白中位数平行,但各组间唾液乳铁蛋白与总蛋白之比无显著差异。在45岁以下的年龄组中,只有DS个体的唾液乳铁蛋白水平中位数较高。同时,45岁以下各组唾液乳铁蛋白水平与总唾液蛋白的比值无显著差异,45岁以上DS受试者的水平低于同龄对照组。此外,与轻度和中度认知障碍组相比,痴呆组DS患者唾液乳铁蛋白水平与总蛋白的比值与认知能力下降有关。综上所述,本研究提示DS患者唾液乳铁蛋白失调,45岁以上的DS患者唾液乳铁蛋白水平与唾液总蛋白的比值显著降低,而45岁以上的DS患者患AD的风险逐渐增加。
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引用次数: 0
Identifying leading anti-inflammatory dietary determinants of depression and loneliness in older adults 确定老年人抑郁和孤独的主要抗炎饮食决定因素
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-21 DOI: 10.1016/j.bbih.2025.101000
Yujia Zhang , Eleonora Iob , Thamara Tapia Munoz

Objectives

The study aims to explore the association between anti-inflammatory dietary variables and prevalence of depression and loneliness in older adults.

Design

A cross-sectional secondary data analysis was performed using data from the English Longitudinal Study of Ageing (ELSA), targeting adults aged 50 and over.

Method

Data from wave 9 of ELSA were utilised. Binary logistic regression was employed to estimate the Odds ratios (ORs) and 95 % confidence intervals (CIs) for the association between participants’ intake of fruits, vegetables, fish, nuts and seeds, legumes, and wholegrains, and the prevalence of depression and loneliness. Two sets of regressions were conducted: the first set examined each dietary component individually, while the second considered all variables simultaneously. Both models were tested with and without adjusting for covariates, including age, gender, ethnicity, self-rated weight, marital status, education, socio-economic status, and activity-limiting long-standing illnesses.

Results

Of 4254 participants included in the analysis, 355 participants (8 %) had depression, and 623 (15 %) reported experiencing loneliness. An association was observed between higher intakes of fruits and lower prevalence of depression (OR = 0.89, 95 % CI: 0.79–1.00, p = 0.05), and between higher intakes of vegetables and lower prevalence of loneliness (OR = 0.91, 95 % CI: 0.83–1.00, p = 0.05). However, these associations lost statistical significance after adjustment for confounders. Similarly, the second model, which included all anti-inflammatory dietary variables, failed to show a significant association with depression and loneliness.

Conclusions

The study does not support the hypothesis that anti-inflammatory variables are associated with prevalence of depression and loneliness in older adults.
目的探讨抗炎饮食变量与老年人抑郁和孤独患病率之间的关系。设计采用英国老龄化纵向研究(ELSA)的数据进行横断面二次数据分析,目标是50岁及以上的成年人。方法利用ELSA第9波数据。采用二元logistic回归来估计参与者摄入水果、蔬菜、鱼类、坚果和种子、豆类和全谷物与抑郁和孤独患病率之间的比值比(ORs)和95%置信区间(ci)。进行了两组回归:第一组单独检查每种饮食成分,而第二组同时考虑所有变量。两种模型都在有和没有调整协变量的情况下进行了测试,协变量包括年龄、性别、种族、自评体重、婚姻状况、教育程度、社会经济地位和限制活动的长期疾病。结果在分析的4254名参与者中,355名参与者(8%)患有抑郁症,623名参与者(15%)报告感到孤独。高水果摄入量与低抑郁患病率之间存在关联(OR = 0.89, 95% CI: 0.79-1.00, p = 0.05),高蔬菜摄入量与低孤独患病率之间存在关联(OR = 0.91, 95% CI: 0.83-1.00, p = 0.05)。然而,在调整混杂因素后,这些关联失去了统计学意义。同样,第二个模型,包括所有抗炎饮食变量,未能显示出抑郁和孤独的显著关联。结论:该研究不支持抗炎变量与老年人抑郁和孤独患病率相关的假设。
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引用次数: 0
Psychoneuroimmunoendocrinological and neuroanatomical basis of suicidal behavior: potential therapeutic strategies with a focus on transcranial magnetic stimulation (TMS) 自杀行为的心理神经免疫内分泌和神经解剖学基础:以经颅磁刺激(TMS)为重点的潜在治疗策略
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-21 DOI: 10.1016/j.bbih.2025.101002
Hesed Virto-Farfan , Gustavo E. Tafet
Suicidal behavior is a complex phenomenon influenced by psychological, environmental, and biological factors. It affects a significant portion of the global population, with more than 720,000 deaths annually and millions of individuals experiencing suicidal ideation. Among those who attempt suicide, only a fraction progresses to a fatal outcome, emphasizing the importance of understanding individual vulnerabilities. This review explores the neuroanatomical basis of suicidal behavior, focusing on key brain regions and potential pathways for neuromodulation therapies, particularly Transcranial Magnetic Stimulation (TMS). The dorsolateral prefrontal cortex (DLPFC) plays a central role in cognitive control and emotional regulation, with extensive connections to the anterior cingulate cortex, amygdala, orbitofrontal cortex, hippocampus, and thalamus. Dysfunctions in these circuits contribute to heightened impulsivity, impaired decision-making, and emotional dysregulation in individuals with suicidal behavior. Structural and functional abnormalities in the DLPFC, coupled with altered neurotransmitter systems and inflammatory markers, have been consistently linked to suicidality. TMS, targeting the left DLPFC, has shown promise in reducing suicidal ideation by modulating frontostriatal connectivity, enhancing neuroplasticity, and improving cortical excitability. High-frequency TMS and accelerated theta-burst stimulation protocols demonstrate rapid therapeutic effects, though further research is needed to establish standardized treatment guidelines. Understanding the anatomical circuits implicated in suicidal behavior provides valuable insights for early risk assessment and the development of targeted neuromodulation interventions aimed at reducing the burden of suicide across diverse psychiatric populations.
自杀行为是一种受心理、环境和生物因素影响的复杂现象。它影响到全球人口的很大一部分,每年有72万多人死亡,数百万人有自杀念头。在那些企图自杀的人中,只有一小部分发展成致命的结果,这强调了了解个人脆弱性的重要性。这篇综述探讨了自杀行为的神经解剖学基础,重点关注神经调节治疗的关键脑区和潜在途径,特别是经颅磁刺激(TMS)。背外侧前额叶皮层(DLPFC)在认知控制和情绪调节中起着核心作用,与前扣带皮层、杏仁核、眶额皮质、海马和丘脑有广泛的联系。这些神经回路的功能障碍导致自杀行为个体的冲动性增强、决策能力受损和情绪失调。DLPFC的结构和功能异常,加上神经递质系统和炎症标志物的改变,一直与自杀有关。针对左侧DLPFC的经颅磁刺激已显示出通过调节额纹状体连通性、增强神经可塑性和改善皮质兴奋性来减少自杀意念的希望。高频经颅磁刺激和加速脑波爆发刺激方案显示出快速的治疗效果,尽管需要进一步的研究来建立标准化的治疗指南。了解与自杀行为有关的解剖回路,为早期风险评估和有针对性的神经调节干预措施的发展提供了有价值的见解,旨在减轻不同精神病人群的自杀负担。
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引用次数: 0
Obesity accelerates age-related memory deficits and alters white matter tract integrity in Ldlr-/-.Leiden mice 肥胖会加速 Ldlr-/-.Leiden 小鼠与年龄相关的记忆缺陷并改变白质束的完整性
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-15 DOI: 10.1016/j.bbih.2025.100991
Florine Seidel , Martine C. Morrison , Ilse Arnoldussen , Vivienne Verweij , Joline Attema , Christa de Ruiter , Wim van Duyvenvoorde , Jessica Snabel , Bram Geenen , Ayla Franco , Maximilian Wiesmann , Robert Kleemann , Amanda J. Kiliaan

Background

Obesity in mid-adulthood has been suggested to promote brain aging and is associated with progressive cognitive impairment later in life. However, the structural and functional alterations that underlie obesity-related cognitive dysfunction are still poorly understood, partly owing to the lack of translational models replicating age- and obesity-related brain pathology.

Methods

The effect of age and high-fat diet (HFD)-induced obesity was investigated in adult Ldlr-/-.Leiden mice, an established translational model for obesity and its comorbidities. During mid-adulthood, from three to eight months of age, brain structure and function (hippocampal volume, cortical thickness, white matter integrity, cerebral blood flow (CBF), resting-state functional connectivity) were monitored with brain magnetic resonance imaging, and cognitive function was evaluated using cognitive tests. Brain pathology was further examined with histopathological and gene expression analyses.

Results

Ldlr-/-.Leiden mice showed age-related decreases in cortical thickness, CBF, brain connectivity, and neurogenesis along with the development of neuroinflammation and (short-term) memory impairments. On HFD feeding, Ldlr-/-.Leiden mice exhibited similar features, but memory deficits started at a younger age than in chow-fed mice. HFD-fed mice additionally showed a rise in CBF with concomitant decline in fractional anisotropy in white matter tracts. Analyses of hippocampal gene expression further revealed an age-related suppression of processes related to metabolic and neuronal function while HFD feeding strongly activated neuroinflammatory pathways.

Conclusions

Ldlr-/-.Leiden mice show similar critical age-related changes in brain structure and function as observed in humans. In this mouse model, HFD feeding particularly trigger disturbances in brain blood perfusion and white matter tract integrity, which may underlie an accelerated cognitive decline in obesity.
研究表明,中年肥胖会促进大脑衰老,并与以后的认知障碍有关。然而,肥胖相关认知功能障碍背后的结构和功能改变仍然知之甚少,部分原因是缺乏复制年龄和肥胖相关脑病理的转化模型。方法探讨年龄和高脂饮食(HFD)诱导的成人Ldlr-/-肥胖的影响。Leiden小鼠,建立了肥胖及其合并症的转化模型。在成年中期,从3到8个月大,用脑磁共振成像监测大脑结构和功能(海马体积、皮质厚度、白质完整性、脑血流量(CBF)、静息状态功能连通性),并使用认知测试评估认知功能。通过组织病理学和基因表达分析进一步检查脑病理。莱顿小鼠表现出与年龄相关的皮层厚度、CBF、大脑连通性和神经发生的减少,并伴有神经炎症和(短期)记忆障碍的发展。在HFD饲喂上,Ldlr-/-。莱顿老鼠也表现出类似的特征,但记忆缺陷开始的年龄比喂食老鼠的要小。饲喂hfd的小鼠CBF增加,同时白质束各向异性分数下降。海马基因表达分析进一步揭示了年龄相关的代谢和神经元功能相关过程的抑制,而HFD喂养强烈激活了神经炎症途径。莱顿小鼠在大脑结构和功能方面表现出与人类相似的与年龄相关的关键变化。在该小鼠模型中,HFD喂养尤其会引发脑血流灌注和白质束完整性的紊乱,这可能是肥胖症认知能力加速下降的基础。
{"title":"Obesity accelerates age-related memory deficits and alters white matter tract integrity in Ldlr-/-.Leiden mice","authors":"Florine Seidel ,&nbsp;Martine C. Morrison ,&nbsp;Ilse Arnoldussen ,&nbsp;Vivienne Verweij ,&nbsp;Joline Attema ,&nbsp;Christa de Ruiter ,&nbsp;Wim van Duyvenvoorde ,&nbsp;Jessica Snabel ,&nbsp;Bram Geenen ,&nbsp;Ayla Franco ,&nbsp;Maximilian Wiesmann ,&nbsp;Robert Kleemann ,&nbsp;Amanda J. Kiliaan","doi":"10.1016/j.bbih.2025.100991","DOIUrl":"10.1016/j.bbih.2025.100991","url":null,"abstract":"<div><h3>Background</h3><div>Obesity in mid-adulthood has been suggested to promote brain aging and is associated with progressive cognitive impairment later in life. However, the structural and functional alterations that underlie obesity-related cognitive dysfunction are still poorly understood, partly owing to the lack of translational models replicating age- and obesity-related brain pathology.</div></div><div><h3>Methods</h3><div>The effect of age and high-fat diet (HFD)-induced obesity was investigated in adult Ldlr-/-.Leiden mice, an established translational model for obesity and its comorbidities. During mid-adulthood, from three to eight months of age, brain structure and function (hippocampal volume, cortical thickness, white matter integrity, cerebral blood flow (CBF), resting-state functional connectivity) were monitored with brain magnetic resonance imaging, and cognitive function was evaluated using cognitive tests. Brain pathology was further examined with histopathological and gene expression analyses.</div></div><div><h3>Results</h3><div>Ldlr-/-.Leiden mice showed age-related decreases in cortical thickness, CBF, brain connectivity, and neurogenesis along with the development of neuroinflammation and (short-term) memory impairments. On HFD feeding, Ldlr-/-.Leiden mice exhibited similar features, but memory deficits started at a younger age than in chow-fed mice. HFD-fed mice additionally showed a rise in CBF with concomitant decline in fractional anisotropy in white matter tracts. Analyses of hippocampal gene expression further revealed an age-related suppression of processes related to metabolic and neuronal function while HFD feeding strongly activated neuroinflammatory pathways.</div></div><div><h3>Conclusions</h3><div>Ldlr-/-.Leiden mice show similar critical age-related changes in brain structure and function as observed in humans. In this mouse model, HFD feeding particularly trigger disturbances in brain blood perfusion and white matter tract integrity, which may underlie an accelerated cognitive decline in obesity.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100991"},"PeriodicalIF":3.7,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848349","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}
引用次数: 0
Mental distress and inflammation in bladder cancer: The nerve makes things less vague 膀胱癌的精神痛苦和炎症:神经使事情变得不那么模糊
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-14 DOI: 10.1016/j.bbih.2025.100995
Iveta Mikolaskova , Yori Gidron , Vladimira Durmanova , Magda Suchankova , Maria Bucova , Luba Hunakova

Objectives

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.

Methods

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.

Results

We found evidence that HRV modulates the relation between perceived stress and inflammation. In patients with low HRV (SDNN <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).

Conclusion

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.
目的探讨膀胱癌患者感知压力、生活满意度、心率变异性(HRV)和免疫炎症标志物之间的相互作用。我们研究了HRV如何调节心理困扰与TNF-α和TGF-β细胞因子水平之间的关系。我们假设高迷走神经活动,正如高HRV所表明的那样,减轻了感知压力和生活不满对炎症的影响。方法对73例膀胱癌患者进行研究。HRV由5分钟心电图记录确定,重点关注正常到正常心跳间隔(SDNN)的标准偏差。采用压力感知量表(PSS)测量心理压力,采用生活满意度问卷(LSQ)评估生活满意度。采用夹心ELISA法检测血清TNF-α浓度和血浆TGF-β水平。结果我们发现HRV调节感知压力和炎症之间的关系。低HRV (SDNN <20 ms)患者PSS与血清TNF-α水平呈正相关,与TGF-β水平呈负相关,而生活满意度与TGF-β呈正相关。这些关系在高HRV患者(SDNN≥20 ms)中不显著。结论高HRV所显示的高迷走神经活动可能减轻心理困扰对膀胱癌患者免疫炎症反应的不利影响。应激相关炎症发生在低HRV条件下,突出了自主调节在癌症预后中的潜在作用。未来的研究应进一步探索这些关系,以制定旨在通过压力管理和增强迷走神经活动来调节癌症炎症的干预措施来改善患者预后。
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引用次数: 0
Social relationships and immune aging in early midlife: Evidence from the National Longitudinal Study of Adolescent to Adult Health
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-12 DOI: 10.1016/j.bbih.2025.100993
Farizah I. Rob , Rebecca C. Stebbins , Jennifer Momkus , Chantel L. Martin , Kathleen Mullan Harris , Allison E. Aiello
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.
免疫系统衰老的特征是t细胞区室的变化,包括naïve t细胞的减少和记忆t细胞的增加。已知压力暴露可预测老年人免疫系统加速老化。然而,通常与压力机制相关的社会关系尚未与这些适应性免疫生物标志物进行广泛研究,特别是在年轻人群中。我们从全国青少年到成人健康纵向研究第五阶段(n = 4451)中,研究了社会关系(数量(社会网络指数、亲密接触指数)和关系质量(配偶/伴侣、朋友和家庭成员)与美国代表性的早期中年人口(33-44岁)免疫衰老之间的联系。使用Wave V期间收集的静脉血样本的DNA甲基化数据计算CD4+记忆:naïve, CD8+记忆:naïve和总CD8+:CD4+ T细胞比率;数值越高,说明免疫特征越老。根据年龄、性别、种族/民族和教育程度调整的调查加权线性回归模型的结果表明,亲密朋友的数量和接触频率越多,与家庭成员的关系越好,与CD4+记忆:幼稚比率的降低有关。CD8+记忆:naïve和CD8+:CD4+比值的结果大多不显著。我们的研究结果表明,在中年之前,更高数量和质量的社会关系可能有助于防止免疫衰老,特别是在CD4+ T细胞区。这强调了在一生中加强社会关系以促进健康长寿的干预措施的重要性。
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引用次数: 0
Depressive symptoms partially mediate the relationship between psychosocial factors and epigenetic age acceleration in a multi-racial/ethnic sample of older adults 在一个多种族/民族的老年人样本中,抑郁症状部分介导了社会心理因素与表观遗传年龄加速之间的关系
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-12 DOI: 10.1016/j.bbih.2025.100994
Lauren A. Opsasnick , Wei Zhao , Lauren L. Schmitz , Scott M. Ratliff , Jessica D. Faul , Xiang Zhou , Belinda L. Needham , Jennifer A. Smith
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.
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.
Psychosocial stress, loneliness, and depressive symptoms were each associated with at least one measure of epigenetic AA (FDR q < 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.

Results

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.
社会心理因素,包括累积的社会心理压力和孤独,与老年人的表观遗传衰老有关。此外,抑郁症状与社会心理因素和表观遗传衰老都有关系。然而,尚不清楚抑郁症状是否介导社会心理因素与表观遗传衰老之间的关联。我们对来自健康与退休研究的2681名老年人(平均年龄:70.4岁)的多种族/民族样本进行了线性回归模型,以检验社会心理压力、孤独和抑郁症状与DNA甲基化估计的五种表观遗传年龄加速(AA)指标之间的关系。对于所有确定的关联,我们测试了性别和受教育程度对效果的影响,并进行了中介分析,以表征抑郁症状在这些关联中的作用。心理社会压力、孤独感和抑郁症状均与至少一种表观遗传AA相关(FDR q <;0.05)。此外,我们观察到孤独、社会心理压力和性别在DunedinPACE上的相互作用,以及孤独和教育程度在GrimAA、PhenoAA和DunedinPACE上的相互作用,女性和没有大学学历的个体对表观遗传衰老的社会心理影响更为敏感。抑郁症状在心理社会压力与HannumAA、GrimAA和DunedinPACE之间的关系中分别起到24%至35%的中介作用,在孤独与GrimAA和DunedinPACE之间的关系中分别起到40%和37%的中介作用。本研究结果可能有助于阐明社会心理因素与表观遗传衰老之间的关系,这对于理解社会心理因素可能导致年龄相关疾病的生物学机制至关重要。
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引用次数: 0
HIV and Low Omega-3 Levels May Heighten Hippocampal Volume Differences Between Men and Women With Substance Use
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-04-05 DOI: 10.1016/j.bbih.2025.100988
Hong Lai , Jiachen Zhuo , Glenn Treisman , Gary Gerstenblith , David D. Celentano , Yihong Yang , Betty Jo Salmeron , Hong Gu , Thorsten M. Leucker , Xiao Liang , Raul N. Mandler , Jag Khalsa , Óscar Peña-Nogales , Shaoguang Chen , Shenghan Lai , Elana Rosenthal , Karl Goodkin , Vincent A. Magnotta

Background

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.

Methods

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).

Results

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 < 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 >0.40 % (p = 0.0003 for ≤0.40 % vs. >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 < 0.00001 for EPA ≤0.40 % vs. >0.40 %; p = 0.004 for DHA ≤2.0 % vs. >2.0 %), and (4) Among Adults with lower episodic memory, higher log-scaled EPA levels were independently associated with greater hippocampal volume.

Conclusions

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.
{"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}
引用次数: 0
Cardiovascular health and its association with dementia, Parkinson's Disease, and mortality among UK older adults
IF 3.7 Q2 IMMUNOLOGY Pub Date : 2025-03-27 DOI: 10.1016/j.bbih.2025.100986
Michael F. Georgescu , May A. Beydoun , Jordan Weiss , Jagdish Kubchandani , Sri Banerjee , Alyssa A. Gamaldo , Michele K. Evans , Alan B. Zonderman

Background

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.

Objectives

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.

Methods

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).

Results

Full Cox models found poor CVH (measured with standardized reverse-coded Life's Essential 8 total score, LE8zrev), to be associated with increased risks for all-cause dementia (Hazard Ratio (HR) = 1.14, 95 % CI: 1.11–1.18, P < 0.001) and all-cause mortality (HR = 1.31, 95 % CI: 1.29–1.33, P < 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 < 0.001), and Healthy→Death (HR = 1.33, 95 % CI: 1.32–1.35, P < 0.001) exhibited a positive relationship with poor CVH.

Conclusions

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.
{"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<sub>zrev</sub>), 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}
引用次数: 0
期刊
Brain, behavior, & immunity - health
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