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A novel analysis of interoceptive underpinnings of anxious psychopathology in COVID-19 survivors 对 COVID-19 幸存者焦虑心理病理学的互感基础进行新的分析。
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-25 DOI: 10.1016/j.bbr.2024.115275

Introduction

SARS-CoV-2 affects brain, body, and their interchange. We investigated interoceptive mechanisms in COVID-19 survivors focusing on their potential link with psychopathology and inflammatory biomarkers.

Methods

We assessed interoceptive accuracy (IAc) and time-perceiving (TA) skills of 57 COVID-19 survivors one month after hospital discharge through, respectively, a heartbeats perception task and a time duration task. Each participant was assessed about his interoceptive awareness (IAw) through Multidimensional Assessment of Interoceptive Awareness questionnaire (MAIA) and then, screened for post-traumatic (Impact of Events Scale – IES-R), anxious (State-Trait Anxiety Inventory – STAI-Y1) and depressive (Zung Self-Rating Depression Scale - ZSDS; Beck Depression Inventory - BDI-13) symptoms.
Biomarkers of inflammation (platelet count, PC; mean platelet volume, MPV and systemic immune-inflammation index, SII) were obtained in a subsample of 40 survivors by a blood sampling conducted at admission and discharge time from the hospital. Correlational, GLM, GLMZ, and mediation analyses were performed.

Results

IAc did not correlate with TA confirming the reliability of interoceptive measure. IAc positively predicts MAIA’s Trusting subscale and negatively predicts anxious psychopathology which fully mediates the effect of IAc on Trusting.PC at hospital admission predicts anxiety at one month after recovery. Again, a higher decrease of SII during hospitalization predicts higher IAc skill and lower anxiety state at one month. The link between SII change and anxiety is fully mediated by IAc.

Conclusions

Our results unveil a potential key role of interoception and brain-body interchange in the exacerbation and maintenance of anxiety psychopathology in COVID-19 survivors.
导言SARS-CoV-2影响大脑、身体和它们之间的相互作用。我们研究了 COVID-19 幸存者的感知机制,重点关注其与精神病理学和炎症生物标志物的潜在联系:我们分别通过心跳感知任务和时间持续任务,评估了 57 名 COVID-19 幸存者出院一个月后的相互感知准确性(IAc)和时间感知能力(TA)。通过多维互感意识评估问卷(MAIA)对每位受试者的互感意识(IAw)进行评估,然后筛查受试者的创伤后症状(事件影响量表-IES-R)、焦虑症状(状态-特质焦虑量表-STAI-Y1)和抑郁症状(Zung抑郁自评量表-ZSDS;贝克抑郁量表-BDI-13)。在入院和出院时对 40 名幸存者的子样本进行血液采样,以获得炎症生物标志物(血小板计数,PC;平均血小板体积,MPV 和全身免疫炎症指数,SII)。研究结果显示,IAc与血红蛋白胆固醇(IAc)和血红蛋白胆固醇(MPV)之间没有相关性:结果:IAc与TA没有相关性,这证实了感知间测量的可靠性。IAc对MAIA的 "信任 "分量表有正向预测作用,对焦虑性精神病理学有负向预测作用,而焦虑性精神病理学又完全调节了IAc对 "信任 "的影响。同样,住院期间 SII 下降越多,则一个月后 IAc 技能越高,焦虑状态越低。SII变化与焦虑之间的联系完全由IAc中介:我们的研究结果揭示了在 COVID-19 存活者的焦虑精神病理学的加剧和维持过程中,内感知和脑体交换可能扮演着关键的角色。
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引用次数: 0
Neurodegeneration: Effects of calorie restriction on the brain sirtuin protein levels 神经退行性变卡路里限制对大脑sirtuin蛋白水平的影响
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-25 DOI: 10.1016/j.bbr.2024.115258

Background

Calorie restriction (CR) is suggested to activate protective mechanisms in neurodegenerative diseases (NDDs). Despite existing literature highlighting the protective role of Sirtuin (SIRT) proteins against age-related neurodegeneration (ND), no study has explored the total levels of SIRT 1, 3, and 6 proteins simultaneously in brain homogenates by ELISA following intermittent calorie restriction. Applying CR protocols in mice to induce stress, we aimed to determine whether ND would be more pronounced with ad libitum (AL) or with CR.

Methods

Mice were randomly assigned to ad libitum (AL), Chronic CR (CCR), or Intermittent CR (ICR) groups at 10 weeks of baseline age (BL). SIRT 1, 3, and 6 protein levels were measured in the homogenized whole-brain supernatants of 49/50 weeks old mice by the ELISA method. Neuronal morphology was evaluated by the cresyl violet on the hippocampus. Neurodegeneration (ND) was assessed by the fluoro-jade and ImageJ was used for quantifications.

Results

In the ICR group, SIRT1 levels were elevated compared to both the AL and BL groups. Similarly, the CCR group exhibited higher SIRT1 values compared to the AL and BL groups. While SIRT3 levels were higher in both the ICR and CCR groups compared to the AL and BL groups, this disparity did not reach statistical significance. SIRT6 levels were also higher in the ICR group compared to both the BL and AL groups, with the CCR group showing higher values compared to the BL and AL groups as well. Image quantification demonstrated significant neurodegeneration in the AL group compared to the CCR and ICR group, with no observed alterations in nerve cell morphology and number.

Conclusion

This study revealed that the levels of SIRT 1, SIRT 3, and SIRT 6 in brain tissue were notably elevated, and there was less evidence of ND at the 50-week mark in groups undergoing continuous calorie restriction and intermittent calorie restriction compared to baseline and ad libitum groups. Our findings illustrate that CR promotes increased SIRT expression in the mouse brain, thereby potentially mitigating neurodegeneration.
背景卡路里限制(CR)被认为能激活神经退行性疾病(NDDs)的保护机制。尽管现有文献强调了 Sirtuin(SIRT)蛋白对年龄相关性神经退行性病变(ND)的保护作用,但还没有研究通过 ELISA 方法同时检测间歇性卡路里限制后脑匀浆中 SIRT 1、3 和 6 蛋白的总含量。我们在小鼠中应用 CR 方案来诱导应激,旨在确定 ND 在自由饮食(AL)或 CR 的情况下是否会更明显。方法:在小鼠基线年龄(BL)为 10 周时,将其随机分配到自由饮食组(AL)、慢性 CR 组(CCR)或间歇 CR 组(ICR)。采用 ELISA 方法测定 49/50 周龄小鼠匀浆全脑上清液中的 SIRT 1、3 和 6 蛋白水平。用甲酚紫对海马的神经元形态进行评估。结果 与 AL 组和 BL 组相比,ICR 组的 SIRT1 水平升高。同样,CCR 组的 SIRT1 值也高于 AL 组和 BL 组。虽然与 AL 组和 BL 组相比,ICR 组和 CCR 组的 SIRT3 水平较高,但这一差异未达到统计学意义。与 BL 组和 AL 组相比,ICR 组的 SIRT6 水平也更高,而 CCR 组的 SIRT6 水平也高于 BL 组和 AL 组。图像定量显示,与 CCR 组和 ICR 组相比,AL 组的神经退行性变明显,但未观察到神经细胞形态和数量的改变。结论这项研究表明,脑组织中的 SIRT 1、SIRT 3 和 SIRT 6 水平明显升高,与基线组和自由组相比,持续热量限制组和间歇热量限制组在 50 周时出现 ND 的证据较少。我们的研究结果表明,CR能促进小鼠大脑中SIRT表达的增加,从而有可能减轻神经退行性变。
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引用次数: 0
Neural mechanisms of cooperation and fairness in iterative prisoner’s dilemma 迭代囚徒困境中合作与公平的神经机制
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-24 DOI: 10.1016/j.bbr.2024.115272
Cooperation is a universal human principle reflecting working with others to achieve common goals. The rational decision-making model contends that cooperation is the best strategy for maximizing benefits in an iterative prisoner’s dilemma. However, the motivations for cooperation (or betrayal) are complex and diverse, and often include fairness reflections. In this study, we used functional magnetic resonance imaging to study underlying neural differences in brain regions related to fairness when people interact with an opponent who tend to cooperate or betray, at different decision-making stages. Results based on 40 university students (25 women) indicate that experiences of cooperation or betrayal affect people’s fairness perception. Distinct neural activities occur in expectation, decision, and outcome phases of decisions. In the expectation phase, those in the cooperative condition exhibited increased activation in the anterior cingulate gyrus, medial superior frontal gyrus, and caudate nucleus compared to those in the uncooperative condition. During the decision phase, those in the cooperative condition showed greater activation in the middle frontal gyrus, caudate nucleus/frontal insula, inferior frontal gyrus, and cingulate gyrus compared to those in the uncooperative condition. In the outcome feedback phase, the caudate nucleus, insula, cingulate gyrus, and inferior frontal gyrus of the orbit were more active in the uncooperative condition than in the cooperative condition. Results also showed a significant correlation between caudate activity and the perception of fairness when expecting uncooperative conditions.
合作是人类的普遍原则,反映了与他人合作以实现共同目标。理性决策模型认为,在迭代的囚徒困境中,合作是实现利益最大化的最佳策略。然而,合作(或背叛)的动机复杂多样,通常还包括公平性的考虑。在这项研究中,我们利用功能磁共振成像技术研究了当人们在不同决策阶段与容易合作或背叛的对手互动时,与公平性相关的脑区的潜在神经差异。基于 40 名大学生(25 名女性)的研究结果表明,合作或背叛的经历会影响人们的公平感知。在决策的预期、决策和结果阶段会出现不同的神经活动。在期望阶段,与不合作者相比,合作者扣带回前部、额叶内侧上回和尾状核的激活增加。在决策阶段,与不合作者相比,合作者额叶中回、尾状核/额叶岛叶、额叶下回和扣带回的激活程度更高。在结果反馈阶段,不合作状态下的尾状核、脑岛、扣带回和眼眶额下回比合作状态下更活跃。结果还显示,在预测不合作条件时,尾状核活动与公平感之间存在明显的相关性。
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引用次数: 0
(2R, 6R)-hydroxynorketamine ameliorates PTSD-like behaviors during the reconsolidation phase of fear memory in rats by modulating the VGF/BDNF/GluA1 signaling pathway in the hippocampus (2R, 6R)-羟基炔诺酮胺通过调节海马中的VGF/BDNF/GluA1信号通路,改善大鼠在恐惧记忆再巩固阶段的创伤后应激障碍样行为
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-24 DOI: 10.1016/j.bbr.2024.115273

Rationale

Fear memory, a fundamental symptom of post-traumatic stress disorder (PTSD), is improved by (2R, 6R)-hydroxynorketamine ((2R, 6R)-HNK) administration. However, the phase of fear memory in which the injected drug is the most effective at mitigating PTSD-like effects remains unknown.

Objective

This study aimed to explore the effects of (2 R, 6 R)-HNK administration during three phases [acquisition (AP), reconsolidation (RP), and extinction (EP)] on PTSD-like behaviors in single prolonged stress (SPS) and contextual fear conditioning (CFC) rat models. The effects of VGF-inducible type of nerve growth factor (VGF), brain-derived neurotrophic factor (BDNF), and GluA1 on hippocampus (HIP) expression were also explored.

Methods

SPS and CFC (SPSC) were used to establish a PTSD rat model. After lateral ventricle injection of 5 μL (2 R, 6 R)-HNK (0.5 nmol). Anxiety-depression-like behaviors were assessed in rats by the open field test (OFT) and elevated plus maze test (EPMT). Situational fear responses were evaluated in rodents by freezing behavior test (FBT) test. In addition, GluA1, VGF, and BDNF were assessed in the hippocampus by Western blot assay (WB) and Immunohistochemistry assay (IF).

Results

SPSC procedure induced PTSD-like behaviors. The SPSC group had decreased spontaneous exploratory behavior and increased fear response. The (2R, 6R)-HNK group showed improved SPSC-induced reduction in GluA1, VGF, and BDNF levels in the HIP. During RP, anxiety and fear avoidance behaviors were alleviated, and the protein levels of GluA1, VGF, and BDNF in the HIP were restored. In contrast, no significant improvement was noted during AP and EP.

Conclusions

(2R,6R)-HNK modulates the VGF/BDNF/GluA1 signaling pathway in the hippocampus and improves PTSD-like behaviors during the reconsolidation phase of fear memory in rats, which may provide a new target for the clinical treatment and prevention of fear-related disorders such as PTSD.
理由恐惧记忆是创伤后应激障碍(PTSD)的一个基本症状,服用(2R, 6R)-hydroxynorketamine((2R, 6R)-HNK)可改善恐惧记忆。本研究旨在探讨在单次延长应激(SPS)和情境恐惧条件反射(CFC)大鼠模型中,在获得(AP)、再巩固(RP)和消退(EP)三个阶段注射(2R, 6R)-HNK对创伤后应激障碍样行为的影响。研究还探讨了VGF诱导型神经生长因子(VGF)、脑源性神经营养因子(BDNF)和GluA1对海马(HIP)表达的影响。侧脑室注射 5 μL (2 R, 6 R)-HNK (0.5 nmol)后,大鼠出现焦虑抑郁样行为。通过开阔地试验(OFT)和高架加迷宫试验(EPMT)对大鼠的焦虑抑郁样行为进行评估。啮齿动物的情境恐惧反应是通过冻结行为试验(FBT)来评估的。此外,还通过 Western 印迹分析(WB)和免疫组化分析(IF)评估了海马中的 GluA1、VGF 和 BDNF。SPSC组的自发探索行为减少,恐惧反应增加。(2R,6R)-HNK组改善了SPSC诱导的HIP中GluA1、VGF和BDNF水平的降低。在 RP 期间,焦虑和恐惧回避行为得到缓解,HIP 中的 GluA1、VGF 和 BDNF 蛋白水平得到恢复。结论(2R,6R)-HNK能调节海马中的VGF/BDNF/GluA1信号通路,改善大鼠在恐惧记忆再巩固阶段的创伤后应激障碍样行为,这可能为临床治疗和预防创伤后应激障碍等恐惧相关疾病提供了新的靶点。
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引用次数: 0
Dynamic brain entropy predicts risky decision-making across transdiagnostic dimensions of psychopathology 大脑动态熵可预测跨诊断层面的精神病理学风险决策
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-24 DOI: 10.1016/j.bbr.2024.115255

Objectives

Maladaptive risky decision-making is a common pathological behavior among patients with various psychiatric disorders. Brain entropy, which measures the complexity of brain time series signals, provides a novel approach to assessing brain health. Despite its potential, the dynamics of brain entropy have seldom been explored. This study aimed to construct a dynamic model of brain entropy and examine its predictive value for risky decision-making in patients with mental disorders, utilizing resting-state functional magnetic resonance imaging (rs-fMRI).

Methods

This study analyzed the rs-fMRI data from a total of 198 subjects, including 48 patients with bipolar disorder (BD), 47 patients with schizophrenia (SZ), 40 patients with adult attention deficit hyperactivity disorder (ADHD), as well as 63 healthy controls (HC). Time series signals were extracted from 264 brain regions based on rs-fMRI. The traditional static entropy and dynamic entropy (coefficient of variation, CV; rate of change, Rate) were constructed, respectively. Support vector regression was employed to predict risky decision-making utilizing leave-one-out cross-validation within each group.

Results

Our findings showed that CV achieved the best performances in HC and BD groups (r = −0.58, MAE = 6.43, R2 = 0.32; r = −0.78, MAE = 12.10, R2 = 0.61), while the Rate achieved the best in SZ and ADHD groups (r = −0.69, MAE = 10.20, R2 = 0.47; r = −0.78, MAE = 7.63, R2 = 0.60). For the dynamic entropy, the feature selection threshold rather than the time window length and overlapping ratio influenced predictive performance.

Conclusions

These results suggest that dynamic brain entropy could be a more effective predictor of risky decision-making than traditional static brain entropy. Our findings offer a novel perspective on exploring brain signal complexity and can serve as a reference for interventions targeting risky decision-making behaviors, particularly in individuals with psychiatric diagnoses.
目的 适应不良的风险决策是各种精神障碍患者的常见病理行为。测量大脑时间序列信号复杂性的脑熵为评估大脑健康提供了一种新方法。尽管脑熵具有潜力,但人们很少对其动态变化进行探索。本研究旨在利用静息态功能磁共振成像(rs-fMRI)构建大脑熵的动态模型,并研究其对精神障碍患者风险决策的预测价值。本研究分析了198名受试者的rs-fMRI数据,其中包括48名双相情感障碍(BD)患者、47名精神分裂症(SZ)患者、40名成人注意缺陷多动障碍(ADHD)患者以及63名健康对照组(HC)。根据 rs-fMRI 从 264 个脑区提取了时间序列信号。分别构建了传统的静态熵和动态熵(变异系数,CV;变化率,Rate)。结果我们的研究结果表明,CV 在 HC 组和 BD 组的表现最好(r = -0.58, MAE = 6.43, R2 = 0.32; r = -0.78, MAE = 12.10, R2 = 0.61),而 Rate 在 SZ 组和 ADHD 组的表现最好(r = -0.69, MAE = 10.20, R2 = 0.47; r = -0.78, MAE = 7.63, R2 = 0.60)。这些结果表明,与传统的静态脑熵相比,动态脑熵可以更有效地预测风险决策。我们的研究结果为探索大脑信号的复杂性提供了一个新的视角,可为针对风险决策行为的干预措施提供参考,尤其是针对精神疾病患者。
{"title":"Dynamic brain entropy predicts risky decision-making across transdiagnostic dimensions of psychopathology","authors":"","doi":"10.1016/j.bbr.2024.115255","DOIUrl":"10.1016/j.bbr.2024.115255","url":null,"abstract":"<div><h3>Objectives</h3><div>Maladaptive risky decision-making is a common pathological behavior among patients with various psychiatric disorders. Brain entropy, which measures the complexity of brain time series signals, provides a novel approach to assessing brain health. Despite its potential, the dynamics of brain entropy have seldom been explored. This study aimed to construct a dynamic model of brain entropy and examine its predictive value for risky decision-making in patients with mental disorders, utilizing resting-state functional magnetic resonance imaging (rs-fMRI).</div></div><div><h3>Methods</h3><div>This study analyzed the rs-fMRI data from a total of 198 subjects, including 48 patients with bipolar disorder (BD), 47 patients with schizophrenia (SZ), 40 patients with adult attention deficit hyperactivity disorder (ADHD), as well as 63 healthy controls (HC). Time series signals were extracted from 264 brain regions based on rs-fMRI. The traditional static entropy and dynamic entropy (coefficient of variation, CV; rate of change, Rate) were constructed, respectively. Support vector regression was employed to predict risky decision-making utilizing leave-one-out cross-validation within each group.</div></div><div><h3>Results</h3><div>Our findings showed that CV achieved the best performances in HC and BD groups (r = −0.58, MAE = 6.43, R<sup>2</sup> = 0.32; r = −0.78, MAE = 12.10, R<sup>2</sup> = 0.61), while the Rate achieved the best in SZ and ADHD groups (r = −0.69, MAE = 10.20, R<sup>2</sup> = 0.47; r = −0.78, MAE = 7.63, R<sup>2</sup> = 0.60). For the dynamic entropy, the feature selection threshold rather than the time window length and overlapping ratio influenced predictive performance.</div></div><div><h3>Conclusions</h3><div>These results suggest that dynamic brain entropy could be a more effective predictor of risky decision-making than traditional static brain entropy. Our findings offer a novel perspective on exploring brain signal complexity and can serve as a reference for interventions targeting risky decision-making behaviors, particularly in individuals with psychiatric diagnoses.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142318770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Remimazolam attenuates lipopolysaccharide-induced neuroinflammation and cognitive dysfunction 雷马唑仑可减轻脂多糖诱发的神经炎症和认知功能障碍
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-23 DOI: 10.1016/j.bbr.2024.115268

Objective

Remimazolam, a novel benzodiazepine, is widely used as an anesthetic in endoscopic procedures; however, its effects on cognitive function remain unclear, limiting its broader application in general anaesthesia. Neuroinflammation is a well-established key factor in the etiology and progression of cognitive dysfunction, including conditions such as Alzheimer's disease, Parkinson's disease, postoperative delirium, and postoperative cognitive dysfunction. Preclinical studies have demonstrated that remimazolam exerts anti-inflammatory and neuroprotective effects, and clinical reports indicate a reduced incidence of postoperative delirium in patients treated with remimazolam. Nevertheless, whether remimazolam improves cognitive function through its anti-inflammatory properties remains uncertain. This study aimed to investigate the neuroprotective effects of remimazolam and its underlying mechanism in a lipopolysaccharide (LPS)-induced model of neuroinflammation, neuronal injury, and cognitive dysfunction

Methods

C57BL/6 J male mice were administered LPS intraperitoneally to establish a model of neuroinflammation-induced cognitive impairment. A subset of mice received remimazolam via intraperitoneal injection 30 minutes prior to LPS administration. Cognitive performance was evaluated using behavioural tests, including the Morris Water Maze (MWM), Novel Object Recognition (NOR) test, and Open Field Test (OFT). Hippocampal tissues were analyzed by haematoxylin-eosin (HE) staining to assess structural changes. Inflammatory markers, including Interleukin (IL)-6, IL-1β, and tumor necrosis factor-α, were quantified using enzyme-linked immunosorbent assay (ELISA) and real-time quantitative PCR. Immunofluorescence was used to detect translocator protein (TSPO) and markers of microglia activation (IBA-1, CD16/32, and CD206).

Results

(1) Remimazolam reversed LPS-induced cognitive deficits, as evidenced by shorter spatial exploration latency and increased platform crossings in the MWM, and an elevated recognition index in the NOR test. (2) Remimazolam improved hippocampal morphology, reducing LPS-induced neuronal damage. (3) Remimazolam significantly decreased levels of hippocampal inflammatory cytokines, inhibited microglial activation, promoted M2-type microglia polarization, and increased TSPO expression.

Conclusion

Remimazolam demonstrated neuroprotective and anti-neuroinflammatory effects in a mouse model of LPS-induced cognitive impairment. These effects are likely mediated through the regulation of TSPO, which inhibits microglial activation and promotes the polarization of microglia from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype.
目的:雷马唑仑是一种新型苯二氮卓类药物,被广泛用作内窥镜手术的麻醉剂;然而,它对认知功能的影响仍不明确,限制了其在全身麻醉中的广泛应用。神经炎症是认知功能障碍(包括阿尔茨海默病、帕金森病、术后谵妄和术后认知功能障碍)的病因和发展过程中一个公认的关键因素。临床前研究表明,雷马唑仑具有抗炎和保护神经的作用,临床报告也显示,接受雷马唑仑治疗的患者术后谵妄的发生率有所降低。然而,雷马唑仑是否能通过其抗炎特性改善认知功能仍不确定。本研究旨在探讨雷马唑仑在脂多糖(LPS)诱导的神经炎症、神经元损伤和认知功能障碍模型中的神经保护作用及其潜在机制 方法:给 C57BL/6J 雄性小鼠腹腔注射 LPS,建立神经炎症诱导的认知功能障碍模型。一部分小鼠在注射 LPS 前 30 分钟腹腔注射雷米马唑仑。小鼠的认知能力通过行为测试进行评估,包括莫里斯水迷宫(MWM)、新物体识别(NOR)测试和开阔地测试(OFT)。海马组织通过血红素-伊红(HE)染色进行分析,以评估结构变化。使用酶联免疫吸附试验(ELISA)和实时定量 PCR 对白细胞介素(IL)-6、IL-1β 和肿瘤坏死因子-α 等炎症标记物进行定量分析。结果:(1)雷米唑仑逆转了LPS诱导的认知缺陷,表现为MWM中空间探索潜伏期缩短、平台穿越增加,以及NOR测试中识别指数升高。(2)雷米唑仑能改善海马形态,减少 LPS 引起的神经元损伤。(3)雷米唑仑能显著降低海马炎症细胞因子水平,抑制小胶质细胞活化,促进M2型小胶质细胞极化,增加TSPO表达:结论:雷米唑仑对 LPS 诱导的认知障碍小鼠模型具有神经保护和抗神经炎症作用。这些作用可能是通过调节 TSPO 来实现的,TSPO 可抑制小胶质细胞活化并促进小胶质细胞从促炎 M1 表型极化到抗炎 M2 表型。
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引用次数: 0
Assessing the association between common functional Nuclear Factor Kappa-b gene polymorphisms (NFKB1, NFKBIZ, NFKBIA) and Alzheimer´s disease 评估常见功能性核因子卡巴-b 基因多态性(NFKB1、NFKBIZ、NFKBIA)与阿尔茨海默病之间的关系
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-23 DOI: 10.1016/j.bbr.2024.115264
The Nuclear Factor Kappa-b (NF-Κb) pathway has been implicated in the pathogenesis of Alzheimer´s disease (AD). We determined whether common variants in the NF-Κb genes were associated with the risk of developing late-onset AD (LOAD). A total of 639 Spanish LOAD and 500 controls were genotyped for the NFKB1 rs28362491/rs7667496, NFKBIA rs696, NFKBIZ rs3217713 and APOE-Ɛ2/3/4 polymorphisms. Rs7667496 C was increased in the patients (p<0.001) with the CC genotype showing a significant risk (CC vs T+, OR= 1.58, 95 %CI=1.25–2.01). The CC genotype was significantly associated with LOAD after correction by APOE-4+ genotypes, age and sex (p=0.0003, OR=1.88, 95 %CI=1.28–2.78). The NFKB1 rs28362491 I - rs7667496 C haplotype was significantly increased in the patients (p=0.02). NFKBIA and NFKBIZ variants were not associated with the risk of LOAD in our population. In conclusion, NFKB1 variants were associated with the risk of LOAD in our population. This finding encourages further studies to determine the involvement of the NF-kB components in LOAD.
核因子卡巴-b(NF-Κb)通路与阿尔茨海默病(AD)的发病机制有关。我们确定了 NF-Κb 基因中的常见变异是否与晚发性阿兹海默症(LOAD)的发病风险有关。我们对 639 名西班牙 LOAD 患者和 500 名对照者进行了 NFKB1 rs28362491/rs7667496、NFKBIA rs696、NFKBIZ rs3217713 和 APOE-Ɛ2/3/4 多态性基因分型。Rs7667496 C 在患者中增加(p<0.001),CC 基因型显示出显著风险(CC vs T+,OR= 1.58,95 %CI=1.25-2.01)。经 APOE-4+ 基因型、年龄和性别校正后,CC 基因型与 LOAD 显著相关(p=0.0003,OR=1.88,95 %CI=1.28-2.78)。患者的 NFKB1 rs28362491 I - rs7667496 C 单倍型显著增加(p=0.02)。在我们的人群中,NFKBIA 和 NFKBIZ 变体与 LOAD 风险无关。总之,在我们的人群中,NFKB1变异与LOAD的风险有关。这一发现有助于进一步研究NF-kB成分在LOAD中的参与情况。
{"title":"Assessing the association between common functional Nuclear Factor Kappa-b gene polymorphisms (NFKB1, NFKBIZ, NFKBIA) and Alzheimer´s disease","authors":"","doi":"10.1016/j.bbr.2024.115264","DOIUrl":"10.1016/j.bbr.2024.115264","url":null,"abstract":"<div><div>The Nuclear Factor Kappa-b (NF-Κb) pathway has been implicated in the pathogenesis of Alzheimer´s disease (AD). We determined whether common variants in the NF-Κb genes were associated with the risk of developing late-onset AD (LOAD). A total of 639 Spanish LOAD and 500 controls were genotyped for the <em>NFKB1</em> rs28362491/rs7667496, <em>NFKBIA</em> rs696, <em>NFKBIZ</em> rs3217713 and <em>APOE-Ɛ2/3/4</em> polymorphisms. Rs7667496 C was increased in the patients (p&lt;0.001) with the CC genotype showing a significant risk (CC vs T+, OR= 1.58, 95 %CI=1.25–2.01). The CC genotype was significantly associated with LOAD after correction by APOE-4+ genotypes, age and sex (p=0.0003, OR=1.88, 95 %CI=1.28–2.78). The <em>NFKB1</em> rs28362491 I - rs7667496 C haplotype was significantly increased in the patients (p=0.02). <em>NFKBIA</em> and <em>NFKBIZ</em> variants were not associated with the risk of LOAD in our population. In conclusion, <em>NFKB1</em> variants were associated with the risk of LOAD in our population. This finding encourages further studies to determine the involvement of the NF-kB components in LOAD.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Novel insights into famotidine as a GSK-3β inhibitor: An explorative study in aluminium chloride-induced Alzheimer’s disease rat model 法莫替丁作为 GSK-3β 抑制剂的新见解:在氯化铝诱导的阿尔茨海默病大鼠模型中进行的探索性研究
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-22 DOI: 10.1016/j.bbr.2024.115270
Alzheimer's disease (AD), a chronic neurodegenerative disease, presents a substantial global health challenge. This study explored the potential therapeutic role of famotidine, a histamine (H2) receptor antagonist, as a glycogen synthase kinase-3β (GSK-3β) inhibitor in the context of AD induced by aluminium chloride (AlCl3) in a rat model. The intricate relationship between GSK-3β dysregulation and AD pathogenesis, particularly in amyloid-β (Aβ) production, formed the basis for investigating famotidine's efficacy. Molecular modelling revealed famotidine's efficient binding to GSK-3β, suggesting inhibitory potential. In behavioural assessments, famotidine-treated groups exhibited dose-dependent improvements in Morris Water Maze, Novel Object Recognition, and Y-Maze tests, comparable to the standard Rivastigmine tartrate group. Biochemical analyses showed that famotidine inhibits acetylcholinesterase, decreases lipid peroxidation, increases antioxidant activity, and mitigates oxidative stress. Moreover, famotidine significantly lowered the levels of GSK-3β, IL-6, and Aβ(1−42). The neuroprotective effects of famotidine were further supported by histopathological analysis. This comprehensive investigation underscores famotidine's potential as a GSK-3β inhibitor, providing insights into its therapeutic impact on AD induced by AlCl3. The study offers a promising avenue for repurposing famotidine due to its established safety profile and widespread availability, highlighting its potential in addressing the formidable challenge of AD.
阿尔茨海默病(AD)是一种慢性神经退行性疾病,给全球健康带来了巨大挑战。本研究探讨了法莫替丁(一种组胺(H2)受体拮抗剂)作为糖原合酶激酶-3β(GSK-3β)抑制剂在大鼠模型中氯化铝(AlCl3)诱导的阿尔茨海默病中的潜在治疗作用。GSK-3β失调与AD发病机制,特别是淀粉样蛋白-β(Aβ)生成之间的复杂关系,是研究法莫替丁疗效的基础。分子建模显示,法莫替丁能与 GSK-3β 有效结合,表明其具有抑制潜力。在行为评估中,法莫替丁治疗组在莫里斯水迷宫、新物体识别和Y-迷宫测试中表现出剂量依赖性改善,与标准酒石酸利伐斯的明组相当。生化分析表明,法莫替丁可抑制乙酰胆碱酯酶,降低脂质过氧化,提高抗氧化活性,减轻氧化应激。此外,法莫替丁还能明显降低 GSK-3β、IL-6 和 Aβ(1-42)的水平。组织病理学分析进一步证实了法莫替丁的神经保护作用。这项全面的研究强调了法莫替丁作为GSK-3β抑制剂的潜力,为其对AlCl3诱导的注意力缺失症的治疗影响提供了深入的见解。这项研究为法莫替丁的再利用提供了一个前景广阔的途径,因为法莫替丁具有公认的安全性和广泛的可获得性,突出了它在应对AD这一严峻挑战方面的潜力。
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引用次数: 0
The brain extracellular space in chronic kidney disease 慢性肾病患者的脑细胞外空间
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-22 DOI: 10.1016/j.bbr.2024.115271
The brain extracellular space (ECS) is a highly complex structure between the innumerable and intermingled processes of brain cells (neurons and glial cells). This space represents up to 20 % of total brain volume (excluding the ventricles) and hosts an extracellular matrix of proteoglycans. The regulation of this space is unclear, though it may differ from other organs due to the presence of the blood brain barrier. Changes in the ECS may modify the diffusion timing of volume-dependent neurotransmitters such as dopamine, thus potentially altering most brain activities. Indeed, recently it has been shown that mild cognitive impairment is correlated to a reduction of ECS. Because water and electrolyte homeostasis are tightly regulated by the kidney, it is possible that a reduced kidney filtration may change the brain extracellular space and therefore explain the reduced cognitive functions exhibited during kidney diseases. The present communication explores the regulation of ECS in the presence of kidney diseases, discussing how reduced kidney function might impact on brain structure and function in both mice and humans, and suggests potential mechanisms for this link.
脑细胞外空间(ECS)是脑细胞(神经元和胶质细胞)无数交错过程之间的一个高度复杂的结构。该空间占大脑总体积的 20%(不包括脑室),并承载着由蛋白聚糖组成的细胞外基质。这一空间的调节机制尚不清楚,但由于存在血脑屏障,它可能与其他器官不同。ECS 的变化可能会改变多巴胺等体积依赖性神经递质的扩散时间,从而可能改变大多数大脑活动。事实上,最近的研究表明,轻度认知障碍与 ECS 的减少有关。由于水和电解质的平衡受到肾脏的严格调节,肾脏过滤功能的降低可能会改变大脑的细胞外空间,从而解释肾脏疾病导致的认知功能降低。本通讯探讨了肾脏疾病对 ECS 的调节,讨论了肾功能减退如何影响小鼠和人类的大脑结构和功能,并提出了这种联系的潜在机制。
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引用次数: 0
The inhibitory control deficit of internet gaming disorder: An Event-Related Potentials(ERPs) study 网络游戏障碍的抑制控制缺陷:事件相关电位(ERPs)研究》。
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-09-21 DOI: 10.1016/j.bbr.2024.115253

Introduction

The primary difficulty and challenge encountered by individuals with Internet Gaming Disorder (IGD) is inhibitory control deficit. Given that different types of inhibitory control have different effects on IGD patients, it is critical to investigate the neurological cognitive processes underlying various inhibitory control problems.

Methods

The IGD-20 questionnaire was used to identify Internet game disorder and healthy control group, and finally Internet game disorder in (n=25) and healthy control group (n=28) in Flanker task, Internet game disorder (n=29) and health control group (n=24) in GO/NOGO task. The Flanker task was employed to investigate distractor interference inhibition control in those with IGD, while the Go/NoGo task was used to measure their prepotent response inhibitory control. Event-related potentials (ERPs) were used to evaluate the brain mechanisms difference of both IGD and healthy participants during these different inhibitory control tasks.

Results

Findings indicate that compared to healthy control subjects, individuals with Internet Gaming Disorder (IGD) have deficits in inhibitory control tasks during both distraction inhibition and prepotent response inhibition tasks, and distraction inhibition occurs earlier than prepotent response inhibition. In distraction inhibition tasks, the IGD group's N2 amplitude is significantly lower than the healthy control groups. In prepotent response inhibition, the N2 amplitude provoked in the IGD group is not only significantly lower than in the healthy control group, but the P3 amplitude is also significantly larger in the IGD group. The main brain activity areas of interference inhibitory control are the frontal lobe and prefrontal lobe, while the main brain activity areas of prepotent response inhibitory control are the frontal lobe and occipital lobe.

Conclusion

The present study concentrates on the differential neurophysiological characteristics observed in individuals with Internet gaming problems, notably the ability to avoid distractions and prepotent reactions. The current research provides foundations for the assessment and development of tailored therapy and treatment methods to address the wide variety of cognitive problems reported in individuals with Internet Gaming Disorder (IGD).
简介网络游戏障碍(IGD)患者遇到的主要困难和挑战是抑制控制能力不足。鉴于不同类型的抑制控制对 IGD 患者的影响不同,研究各种抑制控制问题背后的神经认知过程至关重要:方法:采用 IGD-20 问卷对网络游戏障碍组和健康对照组进行识别,最终在 Flanker 任务中识别出网络游戏障碍组(n=25)和健康对照组(n=28),在 GO/NOGO 任务中识别出网络游戏障碍组(n=29)和健康对照组(n=24)。Flanker任务用于研究IGD患者的分心干扰抑制控制能力,而Go/NoGo任务则用于测量他们的前摄反应抑制控制能力。事件相关电位(ERPs)用于评估 IGD 患者和健康参与者在这些不同的抑制控制任务中大脑机制的差异:研究结果表明,与健康对照组相比,网络游戏障碍(IGD)患者在分心抑制和前能动反应抑制任务中的抑制控制任务中均存在缺陷,且分心抑制发生的时间早于前能动反应抑制。在分心抑制任务中,IGD 组的 N2 振幅明显低于健康对照组。在前能动反应抑制中,IGD 组激起的 N2 振幅不仅明显低于健康对照组,而且 IGD 组的 P3 振幅也明显大于健康对照组。干扰抑制控制的主要脑活动区是额叶和前额叶,而前能动反应抑制控制的主要脑活动区是额叶和枕叶:本研究集中探讨了在网络游戏问题患者身上观察到的不同神经生理学特征,尤其是避免分心的能力和前摄反应。目前的研究为评估和开发有针对性的疗法和治疗方法奠定了基础,以解决网络游戏障碍(IGD)患者的各种认知问题。
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引用次数: 0
期刊
Behavioural Brain Research
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