首页 > 最新文献

Brain, behavior, & immunity - health最新文献

英文 中文
Relationship between body mass index, gray matter volume and peripheral inflammation in patients with post-COVID condition 新冠肺炎后患者体质量指数、灰质体积与外周炎症的关系
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-11-05 DOI: 10.1016/j.bbih.2025.101137
Luise Victoria Claaß , Franziska Schick , Tonia Rocktäschel , Alejandra P. Garza , Christian Gaser , Philipp A. Reuken , Andreas Stallmach , Kathrin Finke , Sharmili Edwin Thanarajah , Martin Walter , Ildiko Rita Dunay , Bianca Besteher , Nils Opel

Background

Obesity, a condition associated with low-grade peripheral inflammation, is an independent risk factor for severe COVID-19 and has been linked to structural brain alterations. Given that post-COVID condition (PCC) is also associated with structural brain abnormalities and lingering immunological alterations, this study aimed to assess whether obesity contributes to these neural and immunological differences in PCC patients.

Methods

We investigated a previously established cohort of PCC patients (n = 61), recruited between April 2021 and June 2022. Whole-brain comparison of gray matter volume (GMV) was conducted by voxel-based morphometry (VBM). Obesity, as measured by body mass index (BMI), as well as age, sex, and total intracranial volume (TIV), were included as regressors in a linear model. Signature immunological markers were quantified in 50 participants using a LEGENDplex™ multiplex bead-based assay.

Results

A significant negative association was found between BMI and GMV in the right thalamus (p(FWE) = 0.039, k = 209, TFCE = 1037.97, x = 18, y = −21, z = 8). Moreover, BMI and thalamic GMV were significantly associated with immunological markers in PCC. Specifically, BMI was positively associated with Interleukin-6 (p = 0.021) and negatively with Interleukin-7 (p = 0.021), while GMV showed positive associations with Interleukin-8 (p = 0.05).

Conclusion

The results suggest that BMI contributes to GMV alterations in PCC patients, with both BMI and GMV demonstrating correlations with peripheral immunological markers. These findings indicate that converging mechanisms involving inflammation and structural brain alterations may contribute to obesity and PCC.
背景:肥胖是一种与低度外周炎症相关的疾病,是严重COVID-19的独立危险因素,与大脑结构改变有关。鉴于新冠肺炎后状态(PCC)也与结构性脑异常和持续的免疫改变有关,本研究旨在评估肥胖是否与PCC患者的这些神经和免疫差异有关。方法:我们调查了先前建立的PCC患者队列(n = 61),于2021年4月至2022年6月招募。全脑灰质体积(GMV)比较采用基于体素的形态测量法(VBM)。通过体重指数(BMI)以及年龄、性别和总颅内容积(TIV)测量的肥胖作为回归因子纳入线性模型。使用基于LEGENDplex™的多重头部检测对50名参与者的特征免疫标记物进行量化。结果BMI与右丘脑GMV呈显著负相关(p(FWE) = 0.039, k = 209, TFCE = 1037.97, x = 18, y = - 21, z = 8)。此外,BMI和丘脑GMV与PCC的免疫标志物显著相关。其中,BMI与白细胞介素-6呈正相关(p = 0.021),与白细胞介素-7呈负相关(p = 0.021), GMV与白细胞介素-8呈正相关(p = 0.05)。结论BMI与PCC患者GMV的改变有关,BMI和GMV均与外周血免疫标志物相关。这些发现表明,涉及炎症和脑结构改变的趋同机制可能导致肥胖和PCC。
{"title":"Relationship between body mass index, gray matter volume and peripheral inflammation in patients with post-COVID condition","authors":"Luise Victoria Claaß ,&nbsp;Franziska Schick ,&nbsp;Tonia Rocktäschel ,&nbsp;Alejandra P. Garza ,&nbsp;Christian Gaser ,&nbsp;Philipp A. Reuken ,&nbsp;Andreas Stallmach ,&nbsp;Kathrin Finke ,&nbsp;Sharmili Edwin Thanarajah ,&nbsp;Martin Walter ,&nbsp;Ildiko Rita Dunay ,&nbsp;Bianca Besteher ,&nbsp;Nils Opel","doi":"10.1016/j.bbih.2025.101137","DOIUrl":"10.1016/j.bbih.2025.101137","url":null,"abstract":"<div><h3>Background</h3><div>Obesity, a condition associated with low-grade peripheral inflammation, is an independent risk factor for severe COVID-19 and has been linked to structural brain alterations. Given that post-COVID condition (PCC) is also associated with structural brain abnormalities and lingering immunological alterations, this study aimed to assess whether obesity contributes to these neural and immunological differences in PCC patients.</div></div><div><h3>Methods</h3><div>We investigated a previously established cohort of PCC patients (n = 61), recruited between April 2021 and June 2022. Whole-brain comparison of gray matter volume (GMV) was conducted by voxel-based morphometry (VBM). Obesity, as measured by body mass index (BMI), as well as age, sex, and total intracranial volume (TIV), were included as regressors in a linear model. Signature immunological markers were quantified in 50 participants using a LEGENDplex™ multiplex bead-based assay.</div></div><div><h3>Results</h3><div>A significant negative association was found between BMI and GMV in the right thalamus (p(FWE) = 0.039, k = 209, TFCE = 1037.97, x = 18, y = −21, z = 8). Moreover, BMI and thalamic GMV were significantly associated with immunological markers in PCC. Specifically, BMI was positively associated with Interleukin-6 (p = 0.021) and negatively with Interleukin-7 (p = 0.021), while GMV showed positive associations with Interleukin-8 (p = 0.05).</div></div><div><h3>Conclusion</h3><div>The results suggest that BMI contributes to GMV alterations in PCC patients, with both BMI and GMV demonstrating correlations with peripheral immunological markers. These findings indicate that converging mechanisms involving inflammation and structural brain alterations may contribute to obesity and PCC.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101137"},"PeriodicalIF":3.5,"publicationDate":"2025-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145521107","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
Serotonin and neurofilament light chain in alcohol-related suicide: Preliminary case observations 5 -羟色胺和酒精相关自杀的神经丝轻链:初步病例观察
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-11-04 DOI: 10.1016/j.bbih.2025.101136
Shao-Cheng Wang , Chih-Hui Wang , Tung-Hsia Liu , Hsian-Wei Kuo , Yu-Li Liu
Alcohol dependence significantly impacts both physiological and psychological health and is strongly linked to increased suicide attempt. However, the neurobiological mechanisms connecting alcohol use disorder (AUD) to suicidality remain inadequately understood. This study evaluated the severity of alcohol dependence in 24 patients diagnosed with AUD using the Alcohol Use Disorders Identification Test (AUDIT). In parallel, peripheral blood levels of neurofilament light chain (NfL), a bioindicator of neuronal injury, and serotonin, a neurotransmitter implicated in mood regulation and suicidality, were quantified. One patient with a prior history of suicide attempts exhibited markedly elevated plasma NfL levels (1350 pg/ml), greatly exceeding the mean observed in non-suicidal AUD patients (33.06 pg/ml). Despite the absence of detectable brain abnormalities on imaging, the patient presented with a lumbar vertebral burst fracture, suggesting spinal cord trauma as the source of neuronal injury. Moreover, serotonin levels in this individual were substantially reduced (89.41 ng/ml) relative to the group average (340.5 ng/ml). These findings suggest that elevated NfL levels may reflect neural injury originating from spinal, rather than cerebral, sources in AUD patients with suicide attempts. Additionally, reduced serotonin levels may serve as a clinically useful bioindicator to stratify suicide attempt in this population.
酒精依赖严重影响生理和心理健康,并与自杀倾向增加密切相关。然而,将酒精使用障碍(AUD)与自杀联系起来的神经生物学机制仍然没有得到充分的了解。本研究使用酒精使用障碍鉴定测试(AUDIT)评估了24例AUD患者的酒精依赖严重程度。同时,对神经损伤的生物指标神经丝轻链(NfL)和血清素(一种涉及情绪调节和自杀倾向的神经递质)的外周血水平进行了量化。一名有自杀企图史的患者血浆NfL水平明显升高(1350 pg/ml),大大超过非自杀性AUD患者的平均值(33.06 pg/ml)。尽管在影像学上没有检测到大脑异常,但患者表现为腰椎爆裂骨折,提示脊髓损伤是神经元损伤的来源。此外,与组平均水平(340.5 ng/ml)相比,该个体的血清素水平显著降低(89.41 ng/ml)。这些发现表明,在自杀未遂的AUD患者中,NfL水平升高可能反映了源自脊柱而非大脑的神经损伤。此外,血清素水平降低可以作为临床上有用的生物指标,对这一人群的自杀企图进行分层。
{"title":"Serotonin and neurofilament light chain in alcohol-related suicide: Preliminary case observations","authors":"Shao-Cheng Wang ,&nbsp;Chih-Hui Wang ,&nbsp;Tung-Hsia Liu ,&nbsp;Hsian-Wei Kuo ,&nbsp;Yu-Li Liu","doi":"10.1016/j.bbih.2025.101136","DOIUrl":"10.1016/j.bbih.2025.101136","url":null,"abstract":"<div><div>Alcohol dependence significantly impacts both physiological and psychological health and is strongly linked to increased suicide attempt. However, the neurobiological mechanisms connecting alcohol use disorder (AUD) to suicidality remain inadequately understood. This study evaluated the severity of alcohol dependence in 24 patients diagnosed with AUD using the Alcohol Use Disorders Identification Test (AUDIT). In parallel, peripheral blood levels of neurofilament light chain (NfL), a bioindicator of neuronal injury, and serotonin, a neurotransmitter implicated in mood regulation and suicidality, were quantified. One patient with a prior history of suicide attempts exhibited markedly elevated plasma NfL levels (1350 pg/ml), greatly exceeding the mean observed in non-suicidal AUD patients (33.06 pg/ml). Despite the absence of detectable brain abnormalities on imaging, the patient presented with a lumbar vertebral burst fracture, suggesting spinal cord trauma as the source of neuronal injury. Moreover, serotonin levels in this individual were substantially reduced (89.41 ng/ml) relative to the group average (340.5 ng/ml). These findings suggest that elevated NfL levels may reflect neural injury originating from spinal, rather than cerebral, sources in AUD patients with suicide attempts. Additionally, reduced serotonin levels may serve as a clinically useful bioindicator to stratify suicide attempt in this population.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101136"},"PeriodicalIF":3.5,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145468665","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
Plasma profiles of neurology-related proteins in at-risk mental state and first-episode psychosis: Associations with psychotic symptoms and cognitive performance 高危精神状态和首发精神病患者的血浆神经学相关蛋白谱:与精神病症状和认知表现的关系
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-11-04 DOI: 10.1016/j.bbih.2025.101134
Martí Llaurador-Coll , Itziar Montalvo , Francesc Estrada , Vanessa Sánchez-Gistau , Henrik Zetterberg , Javier Labad , Andrea L. Benedet , Elisabet Vilella

Background

Early diagnosis of psychosis is crucial, and biomarker detection may provide insights into the pathophysiology of psychosis and the potential for the development of early diagnostic tools. In particular, blood-based proteomic profiling has yielded promising results for psychiatric disorders because of the use of novel high-throughput techniques and the feasibility of performing blood extractions in routine clinical practice.

Study design and methodology

Here, we studied 182 participants (33.3 % females, Xage = 24.66 ± 5.05), comprising 50 healthy controls (HCs), 37 patients with an at-risk mental state (ARMS) and 95 patients with a first episode of psychosis (FEP). We used a panel of 92 neurology-related proteins in a multiplex immunoassay to identify the plasma protein profiles of each group, their coexpression patterns and biological relevance, and their associations with psychotic symptoms and cognitive performance.

Results

CPA2 was overexpressed in both ARMS participants (β = 0.876, adj. p = 0.009) and FEP participants (β = 0.568, adj. p = 0.011) compared with HCs. In FEP participants, in addition to CPA2, 31 other proteins were overexpressed, with GFRA1 being the most differentially expressed protein (β = 1.159, adj. p < 0.001). Coexpression clusters in FEP patients were involved in several biological processes, such as the regulation of myelination, cell adhesion, multicellular organismal processes and axon guidance. In ARMS patients, THY1 expression was inversely correlated with symptom severity (ρ = −0.640, adj. p = 0.039), and IL12 expression was correlated with cognitive performance (ρ = 0.707, adj. p = 0.007); however, no further correlations were found after the false discovery rate adjustment.

Conclusions

Our findings suggest the involvement of CPA2, GFRA1 and IL12, among other neurology-related proteins, in the early phases of psychosis, which, if confirmed, could become promising biomarkers for diagnosis, psychotic symptom development and psychosis-associated cognitive impairment. However, future studies with larger samples, a longitudinal design, and more extensive proteomic panels are needed to validate these biomarkers and refine their clinical applicability.
背景精神病的诊断是至关重要的,生物标志物检测可以提供对精神病病理生理学的见解和早期诊断工具的发展潜力。特别是,基于血液的蛋白质组学分析在精神疾病方面产生了有希望的结果,因为使用了新的高通量技术和在常规临床实践中进行血液提取的可行性。研究设计和方法在这里,我们研究了182名参与者(33.3%为女性,X - age = 24.66±5.05),其中包括50名健康对照(hc), 37名有危险精神状态(ARMS)的患者和95名有首发精神病(FEP)的患者。我们在多重免疫分析中使用了一组92种神经学相关蛋白,以确定每组的血浆蛋白谱、它们的共表达模式和生物学相关性,以及它们与精神病症状和认知表现的关联。结果scpa2在ARMS组(β = 0.876, adj. p = 0.009)和FEP组(β = 0.568, adj. p = 0.011)与hc组相比均过表达。在FEP参与者中,除了CPA2外,还有31种其他蛋白过表达,其中GFRA1是差异表达最多的蛋白(β = 1.159, adj. p < 0.001)。FEP患者的共表达簇参与多个生物学过程,如髓鞘形成、细胞粘附、多细胞有机体过程和轴突引导的调节。在ARMS患者中,THY1表达与症状严重程度呈负相关(ρ = - 0.640, adj. p = 0.039), IL12表达与认知能力相关(ρ = 0.707, adj. p = 0.007);然而,调整错误发现率后,没有发现进一步的相关性。结论研究结果提示CPA2、GFRA1和IL12等神经相关蛋白参与了精神病的早期阶段,如果得到证实,这些蛋白可能成为诊断、精神病症状发展和精神病相关认知障碍的有希望的生物标志物。然而,未来的研究需要更大的样本,纵向设计和更广泛的蛋白质组学面板来验证这些生物标志物并完善其临床适用性。
{"title":"Plasma profiles of neurology-related proteins in at-risk mental state and first-episode psychosis: Associations with psychotic symptoms and cognitive performance","authors":"Martí Llaurador-Coll ,&nbsp;Itziar Montalvo ,&nbsp;Francesc Estrada ,&nbsp;Vanessa Sánchez-Gistau ,&nbsp;Henrik Zetterberg ,&nbsp;Javier Labad ,&nbsp;Andrea L. Benedet ,&nbsp;Elisabet Vilella","doi":"10.1016/j.bbih.2025.101134","DOIUrl":"10.1016/j.bbih.2025.101134","url":null,"abstract":"<div><h3>Background</h3><div>Early diagnosis of psychosis is crucial, and biomarker detection may provide insights into the pathophysiology of psychosis and the potential for the development of early diagnostic tools. In particular, blood-based proteomic profiling has yielded promising results for psychiatric disorders because of the use of novel high-throughput techniques and the feasibility of performing blood extractions in routine clinical practice.</div></div><div><h3>Study design and methodology</h3><div>Here, we studied 182 participants (33.3 % females, <span><math><mrow><mover><mi>X</mi><mo>‾</mo></mover></mrow></math></span><sub>age</sub> = 24.66 ± 5.05), comprising 50 healthy controls (HCs), 37 patients with an at-risk mental state (ARMS) and 95 patients with a first episode of psychosis (FEP). We used a panel of 92 neurology-related proteins in a multiplex immunoassay to identify the plasma protein profiles of each group, their coexpression patterns and biological relevance, and their associations with psychotic symptoms and cognitive performance.</div></div><div><h3>Results</h3><div>CPA2 was overexpressed in both ARMS participants (β = 0.876, adj. p = 0.009) and FEP participants (β = 0.568, adj. p = 0.011) compared with HCs. In FEP participants, in addition to CPA2, 31 other proteins were overexpressed, with GFRA1 being the most differentially expressed protein (β = 1.159, adj. p &lt; 0.001). Coexpression clusters in FEP patients were involved in several biological processes, such as the regulation of myelination, cell adhesion, multicellular organismal processes and axon guidance. In ARMS patients, THY1 expression was inversely correlated with symptom severity (ρ = −0.640, adj. p = 0.039), and IL12 expression was correlated with cognitive performance (ρ = 0.707, adj. p = 0.007); however, no further correlations were found after the false discovery rate adjustment.</div></div><div><h3>Conclusions</h3><div>Our findings suggest the involvement of CPA2, GFRA1 and IL12, among other neurology-related proteins, in the early phases of psychosis, which, if confirmed, could become promising biomarkers for diagnosis, psychotic symptom development and psychosis-associated cognitive impairment. However, future studies with larger samples, a longitudinal design, and more extensive proteomic panels are needed to validate these biomarkers and refine their clinical applicability.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101134"},"PeriodicalIF":3.5,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145468663","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
Natural-cause mortality and C-reactive protein levels in patients with schizophrenia spectrum disorders: A prospective total cohort study 精神分裂症谱系障碍患者的自然原因死亡率和c反应蛋白水平:一项前瞻性全队列研究
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-11-04 DOI: 10.1016/j.bbih.2025.101133
F. Fathian , I. Divkovic , M. Fagerbakke Strømme , A. Mykletun , R.A. Kroken , C.A. Bartz-Johannessen , E. Johnsen

Background

Schizophrenia spectrum disorders (SSD) are associated with an excess mortality risk compared with the general population. The involvement of low-grade inflammation and elevated C-reactive protein (CRP) levels is well established in SSD. However, associations between CRP and mortality risk in SSD are less investigated.

Aim

To investigate the association between the baseline CRP level and natural-cause mortality risk in SSD.

Methods

We included all patients with an SSD diagnosis and baseline CRP measurement from an open cohort study of consecutively admitted patients to a psychiatric acute unit at Haukeland University Hospital, Bergen, Norway, between May 1, 2005 and June 15, 2014. All patients were followed until the time of death or censoring/study end, up to 18.6 years, and only the assessments at admission were the focus of the present study. A competing risk model was used, adjusting for age and sex.

Results

Among 1315 individuals, 245 (19 %) died of natural causes; among these patients, 66 (27 %) deaths were related to cardiovascular disease (CVD). Elevated baseline CRP levels of 1.0 ≤ CRP <3.0 mg/L were significantly associated with increased natural-cause mortality risk (adjusted hazard ratio [AHR], 1.88; 95 % confidence interval [CI], 1.22–2.88; p-value, 0.004), with a stronger association for CRP ≥3.0 mg/L (AHR, 2.28; 95 % CI, 1.50–3.48; p-value, <0.001), compared with patients with CRP <1.0 mg/L. Moreover, baseline CRP ≥3.0 mg/L was associated with increased CVD-related mortality risk (AHR, 3.12; 95 % CI, 1.16–8.41; p-value, 0.024).

Conclusions

Elevated CRP levels were associated with increased natural-cause mortality and, specifically, with CVD-related mortality risk. The CRP level may thus be considered a predictive factor in mortality risk scoring algorithms in SSD.
背景:与普通人群相比,精神分裂症谱系障碍(SSD)与更高的死亡风险相关。低级别炎症和c反应蛋白(CRP)水平升高在SSD中已经得到了很好的证实。然而,关于CRP与SSD患者死亡风险之间关系的研究较少。目的探讨SSD患者CRP基线水平与自然原因死亡风险之间的关系。方法:我们纳入了2005年5月1日至2014年6月15日在挪威卑尔根Haukeland大学医院精神病急症病房连续住院的所有SSD诊断和基线CRP测量的患者。所有患者均被随访至死亡或审查/研究结束,随访时间长达18.6年,仅入院时的评估是本研究的重点。使用了一个竞争风险模型,对年龄和性别进行了调整。结果1315例患者中,自然死亡245例(19%);这些患者中,66例(27%)死亡与心血管疾病(CVD)有关。基线CRP水平升高1.0≤CRP <;3.0 mg/L与自然原因死亡风险增加显著相关(校正危险比[AHR], 1.88; 95%可信区间[CI], 1.22-2.88; p值,0.004),与CRP <;1.0 mg/L患者相比,CRP≥3.0 mg/L的相关性更强(AHR, 2.28; 95% CI, 1.50-3.48; p值,<0.001)。此外,基线CRP≥3.0 mg/L与cvd相关死亡风险增加相关(AHR, 3.12; 95% CI, 1.16-8.41; p值,0.024)。结论:CRP水平升高与自然原因死亡率增加有关,特别是与cvd相关的死亡风险有关。因此,CRP水平可能被认为是SSD死亡风险评分算法的预测因素。
{"title":"Natural-cause mortality and C-reactive protein levels in patients with schizophrenia spectrum disorders: A prospective total cohort study","authors":"F. Fathian ,&nbsp;I. Divkovic ,&nbsp;M. Fagerbakke Strømme ,&nbsp;A. Mykletun ,&nbsp;R.A. Kroken ,&nbsp;C.A. Bartz-Johannessen ,&nbsp;E. Johnsen","doi":"10.1016/j.bbih.2025.101133","DOIUrl":"10.1016/j.bbih.2025.101133","url":null,"abstract":"<div><h3>Background</h3><div>Schizophrenia spectrum disorders (SSD) are associated with an excess mortality risk compared with the general population. The involvement of low-grade inflammation and elevated C-reactive protein (CRP) levels is well established in SSD. However, associations between CRP and mortality risk in SSD are less investigated.</div></div><div><h3>Aim</h3><div>To investigate the association between the baseline CRP level and natural-cause mortality risk in SSD.</div></div><div><h3>Methods</h3><div>We included all patients with an SSD diagnosis and baseline CRP measurement from an open cohort study of consecutively admitted patients to a psychiatric acute unit at Haukeland University Hospital, Bergen, Norway, between May 1, 2005 and June 15, 2014. All patients were followed until the time of death or censoring/study end, up to 18.6 years, and only the assessments at admission were the focus of the present study. A competing risk model was used, adjusting for age and sex.</div></div><div><h3>Results</h3><div>Among 1315 individuals, 245 (19 %) died of natural causes; among these patients, 66 (27 %) deaths were related to cardiovascular disease (CVD). Elevated baseline CRP levels of 1.0 ≤ CRP &lt;3.0 mg/L were significantly associated with increased natural-cause mortality risk (adjusted hazard ratio [AHR], 1.88; 95 % confidence interval [CI], 1.22–2.88; p-value, 0.004), with a stronger association for CRP ≥3.0 mg/L (AHR, 2.28; 95 % CI, 1.50–3.48; p-value, &lt;0.001), compared with patients with CRP &lt;1.0 mg/L. Moreover, baseline CRP ≥3.0 mg/L was associated with increased CVD-related mortality risk (AHR, 3.12; 95 % CI, 1.16–8.41; p-value, 0.024).</div></div><div><h3>Conclusions</h3><div>Elevated CRP levels were associated with increased natural-cause mortality and, specifically, with CVD-related mortality risk. The CRP level may thus be considered a predictive factor in mortality risk scoring algorithms in SSD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101133"},"PeriodicalIF":3.5,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145468667","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
Baicalein alleviates long-term cognitive impairments induced by repeated neonatal sevoflurane exposure via inhibition of cortical microglial TLR4/NF-kB signaling 黄芩素通过抑制皮质小胶质细胞TLR4/NF-kB信号通路,减轻新生儿反复七氟醚暴露引起的长期认知障碍
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-11-03 DOI: 10.1016/j.bbih.2025.101126
Yingqiao Niu , Qiuting Zeng , Yan Yang , Wenbo Liu , Hui Zhang , Shuyu Chen , Xiaomin Li
Sevoflurane, a widely used pediatric anesthetic, has been associated with long-term cognitive impairments following repeated neonatal exposure. Baicalein, a flavonoid derived from Scutellaria baicalensis, exhibits neuroprotective and anti-inflammatory properties. This study evaluated whether baicalein can mitigate sevoflurane-induced neuroinflammation and cognitive deficits in developing rats. Neonatal rats were exposed to sevoflurane (3 %, 2 h/day) from postnatal day (P) 6 to P8. In the intervention group, baicalein (50 mg/kg) was administered intraperitoneally from P6 to P8 and orally via drinking water from P21 to P35. Cognitive performance was assessed between P35 and P40 using the open field test, novel object recognition, and fear conditioning paradigms. Brain tissues were collected for Western blot, ELISA, and immunofluorescence analyses. Baicalein treatment significantly attenuated sevoflurane-induced deficits in memory and learning, particularly in the novel object recognition and fear conditioning tasks. Mechanistically, baicalein inhibited microglial activation, reduced cortical expression of TLR4 and phosphorylated NF-κB p65, and decreased pro-inflammatory mediators including iNOS, IL-1β, and IL-6 at P8. These findings indicate that repeated neonatal sevoflurane exposure impairs cognitive function via microglial-mediated neuroinflammation, and that baicalein's neuroprotective effect is at least partly attributable to modulation of cortical microglial activity via TLR4/NF-κB signaling. This study highlights baicalein as a promising therapeutic strategy to prevent long-term neurodevelopmental deficits in neonates.
七氟醚是一种广泛使用的儿科麻醉剂,与新生儿反复接触后的长期认知障碍有关。黄芩素是从黄芩中提取的黄酮类化合物,具有神经保护和抗炎作用。本研究评估黄芩素是否能减轻七氟醚诱导的大鼠神经炎症和认知缺陷。从出生后第6天至第8天,新生大鼠暴露于七氟醚(3%,2小时/天)。干预组在P6 ~ P8期间腹腔注射黄芩素50 mg/kg,在P21 ~ P35期间通过饮用水口服黄芩素。在P35和P40之间,使用开放场测试、新物体识别和恐惧条件反射范式评估认知表现。收集脑组织进行Western blot、ELISA和免疫荧光分析。黄芩素治疗显著减轻了七氟醚引起的记忆和学习缺陷,特别是在新物体识别和恐惧条件反射任务中。机制上,黄芩素抑制小胶质细胞活化,降低皮层TLR4和磷酸化NF-κB p65的表达,降低促炎介质包括iNOS、IL-1β和IL-6在P8的表达。这些研究结果表明,新生儿反复接触七氟醚可通过小胶质介导的神经炎症损害认知功能,黄芩素的神经保护作用至少部分可归因于TLR4/NF-κB信号通路对皮质小胶质活性的调节。本研究强调黄芩素是预防新生儿长期神经发育缺陷的一种有前景的治疗策略。
{"title":"Baicalein alleviates long-term cognitive impairments induced by repeated neonatal sevoflurane exposure via inhibition of cortical microglial TLR4/NF-kB signaling","authors":"Yingqiao Niu ,&nbsp;Qiuting Zeng ,&nbsp;Yan Yang ,&nbsp;Wenbo Liu ,&nbsp;Hui Zhang ,&nbsp;Shuyu Chen ,&nbsp;Xiaomin Li","doi":"10.1016/j.bbih.2025.101126","DOIUrl":"10.1016/j.bbih.2025.101126","url":null,"abstract":"<div><div>Sevoflurane, a widely used pediatric anesthetic, has been associated with long-term cognitive impairments following repeated neonatal exposure. Baicalein, a flavonoid derived from Scutellaria baicalensis, exhibits neuroprotective and anti-inflammatory properties. This study evaluated whether baicalein can mitigate sevoflurane-induced neuroinflammation and cognitive deficits in developing rats. Neonatal rats were exposed to sevoflurane (3 %, 2 h/day) from postnatal day (P) 6 to P8. In the intervention group, baicalein (50 mg/kg) was administered intraperitoneally from P6 to P8 and orally via drinking water from P21 to P35. Cognitive performance was assessed between P35 and P40 using the open field test, novel object recognition, and fear conditioning paradigms. Brain tissues were collected for Western blot, ELISA, and immunofluorescence analyses. Baicalein treatment significantly attenuated sevoflurane-induced deficits in memory and learning, particularly in the novel object recognition and fear conditioning tasks. Mechanistically, baicalein inhibited microglial activation, reduced cortical expression of TLR4 and phosphorylated NF-κB p65, and decreased pro-inflammatory mediators including iNOS, IL-1β, and IL-6 at P8. These findings indicate that repeated neonatal sevoflurane exposure impairs cognitive function via microglial-mediated neuroinflammation, and that baicalein's neuroprotective effect is at least partly attributable to modulation of cortical microglial activity via TLR4/NF-κB signaling. This study highlights baicalein as a promising therapeutic strategy to prevent long-term neurodevelopmental deficits in neonates.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101126"},"PeriodicalIF":3.5,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145468666","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
Corrigendum to “Induction of endogenous IL-10 promotes resolution and tolerance of nitric oxide in microglia” [Brain Behav. Immun. Health 49 (2025) 101094] “诱导内源性IL-10促进小胶质细胞对一氧化氮的溶解和耐受性”的更正[脑行为]。Immun。卫生49 (2025)101094]
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-11-01 DOI: 10.1016/j.bbih.2025.101116
Hsing-Chun Kuo , Jia-Shing Chen , Chun-Nun Chao , Kam-Fai Lee , Yi-Te Huang , Pin-Cheng Mao , Tzu-Chia Lin , Shu-Chen Chiu , Ya-Ling Huang , Chun-Hsien Chu
{"title":"Corrigendum to “Induction of endogenous IL-10 promotes resolution and tolerance of nitric oxide in microglia” [Brain Behav. Immun. Health 49 (2025) 101094]","authors":"Hsing-Chun Kuo ,&nbsp;Jia-Shing Chen ,&nbsp;Chun-Nun Chao ,&nbsp;Kam-Fai Lee ,&nbsp;Yi-Te Huang ,&nbsp;Pin-Cheng Mao ,&nbsp;Tzu-Chia Lin ,&nbsp;Shu-Chen Chiu ,&nbsp;Ya-Ling Huang ,&nbsp;Chun-Hsien Chu","doi":"10.1016/j.bbih.2025.101116","DOIUrl":"10.1016/j.bbih.2025.101116","url":null,"abstract":"","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101116"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145465878","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
Internalized weight stigma, metabolic syndrome, and inflammation in postmenopausal women with obesity 绝经后肥胖妇女的内化体重耻辱、代谢综合征和炎症
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-11-01 DOI: 10.1016/j.bbih.2025.101129
Rebecca L. Pearl , Stephen D. Anton , Danielle Saunders , Marian Hernandez , Laurie C. Groshon , Miriam Sheynblyum , Dakota L. Leget , Christian McLaren , Sarah Vial , Lecsy Gonzalez , Kevin Wu , Gayane Barsamyan , Thomas A. Wadden

Objective

To determine the relationship of internalized weight stigma with metabolic syndrome (MetS) and markers of inflammation.

Methods

Postmenopausal women with obesity (N = 101) with high or low scores on the Weight Bias Internalization Scale completed a single assessment visit. MetS components (waist circumference, blood pressure, triglycerides, HDL cholesterol, and glucose) were measured, along with body mass index (BMI). Blood samples were drawn to analyze C-reactive protein, interleukin-6, and myeloperoxidase. Participants completed a second measure of internalized weight stigma (Weight Self-Stigma Questionnaire; WSSQ) and reported medications, demographics, depression symptoms, smoking status, and perceived stress (included as covariates).

Results

Logistic regression showed no significant relationship between either measure of internalized weight stigma and MetS when controlling for BMI, depression, and demographics. A small, significant, positive association emerged between WSSQ scores and MetS when adding the covariate of anti-depressant medication (OR = 1.07, p = 0.040). WSSQ scores were associated with significantly greater odds of having high blood pressure (OR = 1.10, p = 0.003) and low HDL cholesterol (OR = 1.06, p = 0.030). Both measures of internalized weight stigma were associated with greater continuous blood pressure values. Inflammatory markers were not associated with internalized weight stigma in most analyses.

Conclusions

Some significant associations were found between internalized weight stigma and MetS components, but more research is needed to clarify these relationships.
目的探讨内化体重耻辱感与代谢综合征(MetS)及炎症标志物的关系。方法体重偏倚内化量表得分高或低的绝经后肥胖妇女(N = 101)完成单次评估访视。代谢当量成分(腰围、血压、甘油三酯、高密度脂蛋白胆固醇和葡萄糖)和身体质量指数(BMI)一起被测量。抽取血样分析c反应蛋白、白细胞介素-6和髓过氧化物酶。参与者完成了第二项内化体重耻辱感的测量(体重自我耻辱感问卷;WSSQ),并报告了药物、人口统计学、抑郁症状、吸烟状况和感知压力(包括作为协变量)。结果logistic回归显示,在控制BMI、抑郁和人口统计学因素的情况下,内化体重耻辱感和MetS之间没有显著关系。当加入抗抑郁药物的协变量时,WSSQ评分与MetS之间出现了小的、显著的正相关(OR = 1.07, p = 0.040)。WSSQ得分与高血压(OR = 1.10, p = 0.003)和低高密度脂蛋白胆固醇(OR = 1.06, p = 0.030)的几率显著增加相关。内化体重耻辱感的两种测量都与较高的连续血压值相关。在大多数分析中,炎症标记物与内化体重耻辱感无关。结论内化体重耻辱感与代谢代谢因子之间存在显著的相关性,但需要更多的研究来阐明这些关系。
{"title":"Internalized weight stigma, metabolic syndrome, and inflammation in postmenopausal women with obesity","authors":"Rebecca L. Pearl ,&nbsp;Stephen D. Anton ,&nbsp;Danielle Saunders ,&nbsp;Marian Hernandez ,&nbsp;Laurie C. Groshon ,&nbsp;Miriam Sheynblyum ,&nbsp;Dakota L. Leget ,&nbsp;Christian McLaren ,&nbsp;Sarah Vial ,&nbsp;Lecsy Gonzalez ,&nbsp;Kevin Wu ,&nbsp;Gayane Barsamyan ,&nbsp;Thomas A. Wadden","doi":"10.1016/j.bbih.2025.101129","DOIUrl":"10.1016/j.bbih.2025.101129","url":null,"abstract":"<div><h3>Objective</h3><div>To determine the relationship of internalized weight stigma with metabolic syndrome (MetS) and markers of inflammation.</div></div><div><h3>Methods</h3><div>Postmenopausal women with obesity (<em>N</em> = 101) with high or low scores on the Weight Bias Internalization Scale completed a single assessment visit. MetS components (waist circumference, blood pressure, triglycerides, HDL cholesterol, and glucose) were measured, along with body mass index (BMI). Blood samples were drawn to analyze C-reactive protein, interleukin-6, and myeloperoxidase. Participants completed a second measure of internalized weight stigma (Weight Self-Stigma Questionnaire; WSSQ) and reported medications, demographics, depression symptoms, smoking status, and perceived stress (included as covariates).</div></div><div><h3>Results</h3><div>Logistic regression showed no significant relationship between either measure of internalized weight stigma and MetS when controlling for BMI, depression, and demographics. A small, significant, positive association emerged between WSSQ scores and MetS when adding the covariate of anti-depressant medication (OR = 1.07, <em>p</em> = 0.040). WSSQ scores were associated with significantly greater odds of having high blood pressure (OR = 1.10, <em>p</em> = 0.003) and low HDL cholesterol (OR = 1.06, <em>p</em> = 0.030). Both measures of internalized weight stigma were associated with greater continuous blood pressure values. Inflammatory markers were not associated with internalized weight stigma in most analyses.</div></div><div><h3>Conclusions</h3><div>Some significant associations were found between internalized weight stigma and MetS components, but more research is needed to clarify these relationships.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101129"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145468083","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
E.coli-derived CsgA-peptides stimulate cytokine production in microglia and lead to transient changes in neocortical Aβ-levels in pre-plaque APPSWE/PS1ΔE9 and wild type mice 大肠杆菌衍生的csga -肽刺激小胶质细胞细胞因子的产生,导致斑块前小鼠APPSWE/PS1ΔE9和野生型小鼠新皮质a - β水平的短暂变化
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-10-23 DOI: 10.1016/j.bbih.2025.101128
Leda Mygind , Gabriel Jensen , Victoria Neesgaard , Katrine Tækker Krohn , Serges Torres Puig , Anders Boysen , Sussanne Petersen , Kate Lykke Lambertsen , Athanasios Metaxas , Michael Kemp , Jakob Møller-Jensen , Bente Finsen
Epidemiological and pre-clinical data propose that infections can accelerate the cognitive decline in Alzheimer's disease (AD) and other dementias. The implication of infectious agents, and especially the role of E.coli and other amyloid-peptide producing bacteria, on the development and progression of cerebral amyloidosis and neuroinflammation, both key neuropathological characteristics of AD, has only been studied to a limited extent.
In this study, recombinant bacterial amyloid surface protein CsgA was injected intracisternally in pre-plaque 8-11-week-old APPSWE/PS1ΔE9 mice and age-matched wild type (WT) mice. Although less potent than bacterial lipopolysaccharide, CsgA significantly increased the gene expression of inflammatory cytokines, such as tumor necrosis factor, in the neocortex of both APPSWE/PS1ΔE9 and WT mice, and in cultured microglia. CsgA exposure also induced transient changes in neocortical amyloid-beta (Aβ) peptide levels, increasing the highly fibrillogenic Aβ42 in the guanidine-fraction in APPSWE/PS1ΔE9 mice and decreasing Aβ40 in the PBS-fraction in WT mice. The changes in Aβ levels had dissipated 24 h post-injection. In line with the only transient changes in Aβ levels and inflammatory gene expression, CsgA did not impact on long term spatial memory in pre-plaque APPSWE/PS1ΔE9 mice.
Our findings highlight a contribution of bacterial amyloid proteins on neuroinflammation and a possible contribution in influencing Aβ-homeostasis during infections. However, findings need to be further elaborated in older APPSWE/PS1ΔE9 mice in which Aβ plaques are abundant and an inflammatory response already established. Also, the impact of CsgA and other bacterial amyloids should be examined after repeated and/or continuous administration and at different concentrations.
流行病学和临床前数据表明,感染可以加速阿尔茨海默病(AD)和其他痴呆症的认知能力下降。感染因子的影响,特别是大肠杆菌和其他产生淀粉样肽的细菌在阿尔茨海默病的主要神经病理特征脑淀粉样变性和神经炎症的发生和进展中的作用,目前只进行了有限的研究。在本研究中,将重组细菌淀粉样蛋白表面蛋白CsgA注入斑块前8-11周龄的APPSWE/PS1ΔE9小鼠和年龄匹配的野生型(WT)小鼠。虽然不如细菌脂多糖有效,但CsgA在APPSWE/PS1ΔE9和WT小鼠的新皮层以及培养的小胶质细胞中显著增加了炎症因子(如肿瘤坏死因子)的基因表达。CsgA暴露还诱导了新皮质淀粉样蛋白- β (Aβ)肽水平的短暂变化,增加了APPSWE/PS1ΔE9小鼠胍-部分的高纤维原性Aβ42,降低了WT小鼠pbs部分的Aβ40。注射24 h后,Aβ水平的变化逐渐消失。与Aβ水平和炎症基因表达的短暂变化一致,CsgA对斑块前APPSWE/PS1ΔE9小鼠的长期空间记忆没有影响。我们的研究结果强调了细菌淀粉样蛋白对神经炎症的贡献,以及在感染期间影响a β稳态的可能贡献。然而,研究结果需要在年龄较大的APPSWE/PS1ΔE9小鼠中进一步阐述,其中Aβ斑块丰富并且已经建立了炎症反应。此外,CsgA和其他细菌淀粉样蛋白的影响应在重复和/或连续给药和不同浓度后进行检查。
{"title":"E.coli-derived CsgA-peptides stimulate cytokine production in microglia and lead to transient changes in neocortical Aβ-levels in pre-plaque APPSWE/PS1ΔE9 and wild type mice","authors":"Leda Mygind ,&nbsp;Gabriel Jensen ,&nbsp;Victoria Neesgaard ,&nbsp;Katrine Tækker Krohn ,&nbsp;Serges Torres Puig ,&nbsp;Anders Boysen ,&nbsp;Sussanne Petersen ,&nbsp;Kate Lykke Lambertsen ,&nbsp;Athanasios Metaxas ,&nbsp;Michael Kemp ,&nbsp;Jakob Møller-Jensen ,&nbsp;Bente Finsen","doi":"10.1016/j.bbih.2025.101128","DOIUrl":"10.1016/j.bbih.2025.101128","url":null,"abstract":"<div><div>Epidemiological and pre-clinical data propose that infections can accelerate the cognitive decline in Alzheimer's disease (AD) and other dementias. The implication of infectious agents, and especially the role of <em>E.coli</em> and other amyloid-peptide producing bacteria, on the development and progression of cerebral amyloidosis and neuroinflammation, both key neuropathological characteristics of AD, has only been studied to a limited extent.</div><div>In this study, recombinant bacterial amyloid surface protein CsgA was injected intracisternally in pre-plaque 8-11-week-old <em>APP</em><sub><em>SWE</em></sub><em>/PS1</em><sub><em>ΔE9</em></sub> mice and age-matched <em>wild type</em> (<em>WT</em>) mice. Although less potent than bacterial lipopolysaccharide, CsgA significantly increased the gene expression of inflammatory cytokines, such as tumor necrosis factor, in the neocortex of both <em>APP</em><sub><em>SWE</em></sub><em>/PS1</em><sub><em>ΔE9</em></sub> and <em>WT</em> mice, and in cultured microglia. CsgA exposure also induced transient changes in neocortical amyloid-beta (Aβ) peptide levels, increasing the highly fibrillogenic Aβ<sub>42</sub> in the guanidine-fraction in <em>APP</em><sub><em>SWE</em></sub><em>/PS1</em><sub><em>ΔE9</em></sub> mice and decreasing Aβ<sub>40</sub> in the PBS-fraction in <em>WT</em> mice. The changes in Aβ levels had dissipated 24 h post-injection. In line with the only transient changes in Aβ levels and inflammatory gene expression, CsgA did not impact on long term spatial memory in pre-plaque <em>APP</em><sub><em>SWE</em></sub><em>/PS1</em><sub><em>ΔE9</em></sub> mice.</div><div>Our findings highlight a contribution of bacterial amyloid proteins on neuroinflammation and a possible contribution in influencing Aβ-homeostasis during infections. However, findings need to be further elaborated in older <em>APP</em><sub><em>SWE</em></sub><em>/PS1</em><sub><em>ΔE9</em></sub> mice in which Aβ plaques are abundant and an inflammatory response already established. Also, the impact of CsgA and other bacterial amyloids should be examined after repeated and/or continuous administration and at different concentrations.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101128"},"PeriodicalIF":3.5,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145428835","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
Preventing effect of plant extracts and omega-3 on age-related cognitive decline in male mice 植物提取物和omega-3对雄性小鼠衰老相关认知衰退的预防作用
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-10-23 DOI: 10.1016/j.bbih.2025.101127
Marie Martin , Adrien Peltier , Heena Vanmalibhai Lad , Aline Foury , Charlotte Madore-Delpech , Line Pourtau , David Gaudout , Sophie Layé , Véronique Pallet , Anne-Laure Dinel , Corinne Joffre

Background

Aging is associated with cognitive decline, accompanied by neuroinflammation, oxidative stress, impaired synaptic plasticity, and gut microbiota dysbiosis. Nutritional interventions, specifically those rich in polyphenols, carotenoids, and omega-3 (om-3) fatty acids, have demonstrated potential benefits in preventing age-related cognitive decline. This study investigates the combined effects of plant extracts (PE) including polyphenols and carotenoids, and fish oil containing om-3 on cognitive function and underlying biological processes in aged mice.

Objectives

To assess the impact of PE and om-3, alone and in combination, on age-related cognitive decline, especially on memory outcomes and to highlight mechanisms involved in these effects.

Methods

17-month-old male C57BL/6 J mice were divided into control and supplemented groups (PE, om-3, and PE + om-3). A group of young mice was used for positive control. Behavioral assessments, including the Elevated Plus Maze (EPM) for anxiety-like behavior, the Object Location Test (OLT) for short-term memory and the Morris Water Maze (MWM) for long-term memory, were conducted. RNA sequencing, fatty acid and oxylipin concentrations analysis and gut microbiota analysis were used to explore molecular changes and microbial diversity.

Results

All supplementations significantly improved short-term memory in the OLT, while only PE and PE + om-3 prevented long-term memory deficits in the MWM. All supplementations modulated gene expression, reducing inflammation, apoptosis or oxidative stress markers in the hippocampus. PE + om-3 further enhanced synaptic plasticity pathways and improved microbiota composition by decreasing harmful bacteria associated with cognitive decline.

Conclusion

Combined PE and om-3 supplementation could provide a complementary approach to combat age-related cognitive decline, highlighting its potential in promoting long-term neuroprotection through modulation of inflammation, oxidative stress and gut microbiota.
衰老与认知能力下降有关,并伴有神经炎症、氧化应激、突触可塑性受损和肠道微生物群失调。营养干预,特别是那些富含多酚、类胡萝卜素和omega-3脂肪酸的营养干预,已经证明在预防与年龄相关的认知能力下降方面有潜在的好处。本研究探讨了含多酚类胡萝卜素的植物提取物(PE)和含om-3的鱼油对老年小鼠认知功能和潜在生物学过程的联合影响。目的评估PE和om-3单独或联合对年龄相关认知衰退的影响,特别是对记忆结果的影响,并强调这些影响的机制。方法将17月龄雄性C57BL/ 6j小鼠分为PE组、om-3组和PE + om-3组。一组幼鼠作为阳性对照。行为评估包括焦虑样行为的高架+迷宫(EPM)、短期记忆的物体定位测试(OLT)和长期记忆的莫里斯水迷宫(MWM)。利用RNA测序、脂肪酸和氧脂质浓度分析和肠道微生物群分析来探索分子变化和微生物多样性。结果所有补品均能显著改善大鼠的短期记忆,而只有PE和PE + om-3能预防大鼠的长期记忆缺陷。所有补充剂都可以调节基因表达,减少海马中的炎症、细胞凋亡或氧化应激标志物。PE + om-3通过减少与认知能力下降相关的有害细菌,进一步增强了突触可塑性通路,改善了微生物群组成。结论PE和om-3联合补充可提供对抗年龄相关认知衰退的补充方法,强调其通过调节炎症、氧化应激和肠道微生物群来促进长期神经保护的潜力。
{"title":"Preventing effect of plant extracts and omega-3 on age-related cognitive decline in male mice","authors":"Marie Martin ,&nbsp;Adrien Peltier ,&nbsp;Heena Vanmalibhai Lad ,&nbsp;Aline Foury ,&nbsp;Charlotte Madore-Delpech ,&nbsp;Line Pourtau ,&nbsp;David Gaudout ,&nbsp;Sophie Layé ,&nbsp;Véronique Pallet ,&nbsp;Anne-Laure Dinel ,&nbsp;Corinne Joffre","doi":"10.1016/j.bbih.2025.101127","DOIUrl":"10.1016/j.bbih.2025.101127","url":null,"abstract":"<div><h3>Background</h3><div>Aging is associated with cognitive decline, accompanied by neuroinflammation, oxidative stress, impaired synaptic plasticity, and gut microbiota dysbiosis. Nutritional interventions, specifically those rich in polyphenols, carotenoids, and omega-3 (om-3) fatty acids, have demonstrated potential benefits in preventing age-related cognitive decline. This study investigates the combined effects of plant extracts (PE) including polyphenols and carotenoids, and fish oil containing om-3 on cognitive function and underlying biological processes in aged mice.</div></div><div><h3>Objectives</h3><div>To assess the impact of PE and om-3, alone and in combination, on age-related cognitive decline, especially on memory outcomes and to highlight mechanisms involved in these effects.</div></div><div><h3>Methods</h3><div>17-month-old male C57BL/6 J mice were divided into control and supplemented groups (PE, om-3, and PE + om-3). A group of young mice was used for positive control. Behavioral assessments, including the Elevated Plus Maze (EPM) for anxiety-like behavior, the Object Location Test (OLT) for short-term memory and the Morris Water Maze (MWM) for long-term memory, were conducted. RNA sequencing, fatty acid and oxylipin concentrations analysis and gut microbiota analysis were used to explore molecular changes and microbial diversity.</div></div><div><h3>Results</h3><div>All supplementations significantly improved short-term memory in the OLT, while only PE and PE + om-3 prevented long-term memory deficits in the MWM. All supplementations modulated gene expression, reducing inflammation, apoptosis or oxidative stress markers in the hippocampus. PE + om-3 further enhanced synaptic plasticity pathways and improved microbiota composition by decreasing harmful bacteria associated with cognitive decline.</div></div><div><h3>Conclusion</h3><div>Combined PE and om-3 supplementation could provide a complementary approach to combat age-related cognitive decline, highlighting its potential in promoting long-term neuroprotection through modulation of inflammation, oxidative stress and gut microbiota.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101127"},"PeriodicalIF":3.5,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145363583","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
Altered immune and inflammatory gene expression in prefrontal cortex of antipsychotic-free schizophrenia subjects 无抗精神病药物的精神分裂症患者前额叶皮层免疫和炎症基因表达的改变
IF 3.5 Q2 IMMUNOLOGY Pub Date : 2025-10-14 DOI: 10.1016/j.bbih.2025.101125
Sergi Mas , Xabier Elcoroaristizabal-Martín , Carlos Cortijo Bringas , Benito Morentin , Luis F. Callado , J. Javier Meana , Guadalupe Rivero
Gene expression studies in dorsolateral prefrontal cortex (DLPFC) of subjects with schizophrenia have repeatedly reported alterations in immune and inflammatory responses as well as neuronal and mitochondrial processes. Whether the findings are due to schizophrenia and/or to the effect of antipsychotic (AP) drug exposure is particularly intriguing.
In the present study, we performed a transcriptomic study in DLPFC of 16 schizophrenia subjects with no detectable AP blood levels at the time of death. Each schizophrenia subject was matched to a control subject for sex, age, postmortem interval and storage time of the samples. Weighted co-expression network analysis (WGCNA) of transcriptomic data identified 33 modules of co-expressed genes. One of these modules was significantly associated with schizophrenia diagnosis. Protein-protein interaction networks were built within the genes in the module and submitted to gene set enrichment analysis on biological processes. Results revealed the implication of immune and inflammatory responses, cytoskeleton regulation, neurotrophic factors and protein post-translational modifications. Analysis of the promoter regions of the clustered genes predicted the enrichment of 6 transcription factors, including SP1, previously associated with schizophrenia.
Present results in DLPFC of AP-free schizophrenia subjects indicate that the identified biological processes, especially immune and inflammatory response alterations are representative of schizophrenia disorder and not a mere effect of acute AP exposure.
对精神分裂症患者背外侧前额叶皮层(DLPFC)基因表达的研究已经多次报道了免疫和炎症反应以及神经元和线粒体过程的改变。这一发现是由于精神分裂症和/或抗精神病药物(AP)的影响,这是特别有趣的。在本研究中,我们对16名精神分裂症患者的DLPFC进行了转录组学研究,这些患者在死亡时血液中没有检测到AP水平。每个精神分裂症受试者在性别、年龄、死后间隔和样本保存时间上与对照受试者相匹配。加权共表达网络分析(WGCNA)转录组数据确定了33个共表达基因模块。其中一个模块与精神分裂症诊断显著相关。在模块内的基因内建立蛋白质-蛋白质相互作用网络,并提交给生物过程的基因集富集分析。结果揭示了免疫和炎症反应、细胞骨架调节、神经营养因子和蛋白质翻译后修饰的影响。对聚集基因的启动子区域的分析预测了6个转录因子的富集,包括SP1,之前与精神分裂症相关。目前对无AP精神分裂症患者DLPFC的研究结果表明,已确定的生物学过程,特别是免疫和炎症反应的改变是精神分裂症的代表,而不仅仅是急性AP暴露的影响。
{"title":"Altered immune and inflammatory gene expression in prefrontal cortex of antipsychotic-free schizophrenia subjects","authors":"Sergi Mas ,&nbsp;Xabier Elcoroaristizabal-Martín ,&nbsp;Carlos Cortijo Bringas ,&nbsp;Benito Morentin ,&nbsp;Luis F. Callado ,&nbsp;J. Javier Meana ,&nbsp;Guadalupe Rivero","doi":"10.1016/j.bbih.2025.101125","DOIUrl":"10.1016/j.bbih.2025.101125","url":null,"abstract":"<div><div>Gene expression studies in dorsolateral prefrontal cortex (DLPFC) of subjects with schizophrenia have repeatedly reported alterations in immune and inflammatory responses as well as neuronal and mitochondrial processes. Whether the findings are due to schizophrenia and/or to the effect of antipsychotic (AP) drug exposure is particularly intriguing.</div><div>In the present study, we performed a transcriptomic study in DLPFC of 16 schizophrenia subjects with no detectable AP blood levels at the time of death. Each schizophrenia subject was matched to a control subject for sex, age, postmortem interval and storage time of the samples. Weighted co-expression network analysis (WGCNA) of transcriptomic data identified 33 modules of co-expressed genes. One of these modules was significantly associated with schizophrenia diagnosis. Protein-protein interaction networks were built within the genes in the module and submitted to gene set enrichment analysis on biological processes. Results revealed the implication of immune and inflammatory responses, cytoskeleton regulation, neurotrophic factors and protein post-translational modifications. Analysis of the promoter regions of the clustered genes predicted the enrichment of 6 transcription factors, including SP1, previously associated with schizophrenia.</div><div>Present results in DLPFC of AP-free schizophrenia subjects indicate that the identified biological processes, especially immune and inflammatory response alterations are representative of schizophrenia disorder and not a mere effect of acute AP exposure.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101125"},"PeriodicalIF":3.5,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145363584","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
期刊
Brain, behavior, & immunity - health
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1