Pub Date : 2026-02-01Epub Date: 2025-12-22DOI: 10.1016/j.bbih.2025.101166
Folkert H. van Bruggen , Roger S. McIntyre
Bipolar disorder (BD) and major depressive disorder (MDD) are highly prevalent, disabling psychiatric illnesses marked by substantial heterogeneity and frequent metabolic and inflammatory comorbidities. Growing evidence implicates low-grade inflammation, immune dysregulation, and insulin resistance (IR) in the pathophysiology, progression, and treatment response of mood disorders. While numerous clinical trials have investigated immunometabolic targeted interventions, outcomes have been inconsistent, due to limited stratification of participants based on underlying biology. This perspective paper aims to identify practical biomarkers and biosignatures to guide patient selection and optimize immunometabolic trial design. We summarize evidence linking neuroinflammation and IR to illness burden, discuss clinical trials targeting these mechanisms, and highlight emerging markers, including extracellular vesicles, monocyte gene expression profiles, and neuron-derived vesicle signatures of IR. No single validated biomarker for identification of immunometabolic phenotype currently exists, but multimodal biosignatures combining genetic, epigenetic, proteomic, and clinical features offer a pragmatic empirical path forward. Integrating these markers with advanced analytic approaches, such as machine learning, holds promise for identifying biologically coherent subgroups most likely to benefit from targeted immunometabolic interventions, accelerating precision medicine for BD and MDD.
{"title":"Neuroinflammation and insulin resistance in major depression and bipolar disorder: Implications for clinical trials evaluating immunometabolic targeted therapies","authors":"Folkert H. van Bruggen , Roger S. McIntyre","doi":"10.1016/j.bbih.2025.101166","DOIUrl":"10.1016/j.bbih.2025.101166","url":null,"abstract":"<div><div>Bipolar disorder (BD) and major depressive disorder (MDD) are highly prevalent, disabling psychiatric illnesses marked by substantial heterogeneity and frequent metabolic and inflammatory comorbidities. Growing evidence implicates low-grade inflammation, immune dysregulation, and insulin resistance (IR) in the pathophysiology, progression, and treatment response of mood disorders. While numerous clinical trials have investigated immunometabolic targeted interventions, outcomes have been inconsistent, due to limited stratification of participants based on underlying biology. This perspective paper aims to identify practical biomarkers and biosignatures to guide patient selection and optimize immunometabolic trial design. We summarize evidence linking neuroinflammation and IR to illness burden, discuss clinical trials targeting these mechanisms, and highlight emerging markers, including extracellular vesicles, monocyte gene expression profiles, and neuron-derived vesicle signatures of IR. No single validated biomarker for identification of immunometabolic phenotype currently exists, but multimodal biosignatures combining genetic, epigenetic, proteomic, and clinical features offer a pragmatic empirical path forward. Integrating these markers with advanced analytic approaches, such as machine learning, holds promise for identifying biologically coherent subgroups most likely to benefit from targeted immunometabolic interventions, accelerating precision medicine for BD and MDD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101166"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939123","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}
Pub Date : 2026-02-01Epub Date: 2025-12-11DOI: 10.1016/j.bbih.2025.101158
Monica T. Jones , Rachael A. Cronin , Mathew D. Marques , Matthias Weigl , Nicolas Rohleder , Linda Becker , Helena C. Kaltenegger , Bradley J. Wright
Objective
Chronic low-grade inflammation may help explain the relationship between stress, well-being, and disease, but the pathway and temporal order have not yet been tested prospectively. To understand the pathways between perceived stress, well-being, C-reactive protein, and hair cortisol, we investigated the temporal ordering of these variables in a sample of hospital employees.
Methods
Random-intercepts cross-lagged panel models were conducted using three 6-monthly waves of data collected from new employees at a German hospital (N = 296, 77.7 % female, M age = 28.59) in a prospective cohort study. Self-reported data on perceived stress and well-being, hair strands for hair cortisol concentration, and capillary blood samples for C-reactive protein were collected for analysis.
Results
While our study did not support a causal relationship between changes in stress levels and later changes in either hair cortisol or low-grade inflammation, we provide evidence to suggest that increases in perceived stress led to later decreases in well-being. In contrast, changes in well-being did not predict changes in perceived stress levels.
Conclusion
This is the first prospective repeated-measure study to examine the temporal associations between stress, well-being, hair cortisol concentrations, and chronic low-grade inflammation. Our analyses suggest that perceived stress in this sample precedes changes in well-being, highlighting the importance of prevention and early intervention.
{"title":"Perceived stress precedes declines in Well-being: A prospective study of stress, well-being, hair cortisol, and low-grade inflammation in hospital employees","authors":"Monica T. Jones , Rachael A. Cronin , Mathew D. Marques , Matthias Weigl , Nicolas Rohleder , Linda Becker , Helena C. Kaltenegger , Bradley J. Wright","doi":"10.1016/j.bbih.2025.101158","DOIUrl":"10.1016/j.bbih.2025.101158","url":null,"abstract":"<div><h3>Objective</h3><div>Chronic low-grade inflammation may help explain the relationship between stress, well-being, and disease, but the pathway and temporal order have not yet been tested prospectively. To understand the pathways between perceived stress, well-being, C-reactive protein, and hair cortisol, we investigated the temporal ordering of these variables in a sample of hospital employees.</div></div><div><h3>Methods</h3><div>Random-intercepts cross-lagged panel models were conducted using three 6-monthly waves of data collected from new employees at a German hospital (<em>N</em> = 296, 77.7 % female, M age = 28.59) in a prospective cohort study. Self-reported data on perceived stress and well-being, hair strands for hair cortisol concentration, and capillary blood samples for C-reactive protein were collected for analysis.</div></div><div><h3>Results</h3><div>While our study did not support a causal relationship between changes in stress levels and later changes in either hair cortisol or low-grade inflammation, we provide evidence to suggest that increases in perceived stress led to later decreases in well-being. In contrast, changes in well-being did not predict changes in perceived stress levels.</div></div><div><h3>Conclusion</h3><div>This is the first prospective repeated-measure study to examine the temporal associations between stress, well-being, hair cortisol concentrations, and chronic low-grade inflammation. Our analyses suggest that perceived stress in this sample precedes changes in well-being, highlighting the importance of prevention and early intervention.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101158"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798680","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}
Pub Date : 2026-02-01Epub Date: 2025-12-01DOI: 10.1016/j.bbih.2025.101156
Wilson Vincent , Annesa Flentje , Benjamin S. Dominguez , Robert H. Paul , Savita Pahwa , Suresh Pallikkuth , Margaret Roach , Dietmar Fuchs , Samantha E. Dilworth , Torsten B. Neilands , Peter W. Hunt , Gowri Sunder , Cody Lentz , Sydney Telaak , Adam W. Carrico
Background
Microbial translocation, immune activation, inflammation, and dysregulated metabolism of neurotransmitter precursors are interacting pathophysiologic processes linked to neuropsychiatric comorbidities and faster HIV disease progression. We examined correlates of distinct phenotypes of gut-immune dysregulation in people living with HIV (PWH) who use methamphetamine.
Methods
Participants were 122 PWH who had biochemically confirmed recent methamphetamine use, including non-injection use. Peripheral plasma markers reflected: intestinal permeability, microbial translocation, immune activation, inflammation, and dysregulated metabolism of neurotransmitter precursors. Using latent profile analysis (i.e., clustering) of these markers, we identified gut-immune phenotypes and their clinical, demographic, and stigma-related correlates.
Results
Three immune profiles emerged: (1) low gut-immune dysregulation with lower microbial translocation, macrophage activation, inflammation, and tryptophan catabolism; (2) moderate gut-immune dysregulation with all markers within average range; and (3) high gut-immune dysregulation with higher microbial translocation, immune activation, inflammation, and tryptophan catabolism. In adjusted analyses, higher viral load (one log10 copy/ml; AOR = 1.97, 95 % CI = 1.02–3.82), injection of methamphetamine (AOR = 3.60, 95 % CI = 1.23–10.50), and internalized stigma (AOR = 1.78, 95 % CI = 1.01–3.15) were associated with having a moderate gut-immune dysregulation profile. Additionally, higher viral load (AOR = 2.98, 95 % CI = 1.53–5.24) and injecting methamphetamine (AOR = 5.45, 95 % CI = 1.34–17.78) were associated with having a high gut-immune dysregulation profile.
Conclusions
Distinct patterns of microbial translocation, immune activation, inflammation, and metabolism of amino acid precursors distinguished gut-immune phenotypes of PWH reporting injection methamphetamine use and greater internalized stigma. Interventions tailored to PWH who inject methamphetamine or struggle with internalized stigma could optimize HIV-related health outcomes.
微生物易位、免疫激活、炎症和神经递质前体代谢失调是与神经精神合并症和更快的HIV疾病进展相关的相互作用的病理生理过程。我们研究了使用甲基苯丙胺的HIV感染者（PWH）肠道免疫失调的不同表型的相关性。方法研究对象为122名生物化学证实近期使用甲基苯丙胺（包括非注射使用）的PWH。外周血浆标志物反映：肠道通透性、微生物易位、免疫激活、炎症和神经递质前体代谢失调。利用这些标记物的潜在特征分析（即聚类），我们确定了肠道免疫表型及其临床、人口统计学和耻感相关因素。结果出现了三种免疫特征：(1)低肠道免疫失调，微生物易位、巨噬细胞激活、炎症和色氨酸分解代谢降低；(2)中度肠道免疫失调，各项指标均在平均范围内；(3)肠道免疫高度失调，微生物易位、免疫激活、炎症和色氨酸分解代谢增加。在校正分析中，较高的病毒载量（1 log10拷贝/ml； AOR = 1.97, 95% CI = 1.02-3.82）、注射甲基苯丙胺（AOR = 3.60, 95% CI = 1.23-10.50）和内化病耻感（AOR = 1.78, 95% CI = 1.01-3.15）与中度肠道免疫失调相关。此外，较高的病毒载量（AOR = 2.98, 95% CI = 1.53-5.24）和注射甲基苯丙胺（AOR = 5.45, 95% CI = 1.34-17.78）与较高的肠道免疫失调相关。结论不同的微生物易位、免疫激活、炎症和氨基酸前体代谢模式区分了PWH报告注射甲基苯丙胺的肠道免疫表型和更大的内化耻感。针对注射甲基苯丙胺或与内在耻辱作斗争的PWH量身定制的干预措施可以优化与艾滋病毒相关的健康结果。
{"title":"Body talk: Correlates of gut-immune dysregulation phenotypes in people living with HIV who use methamphetamine","authors":"Wilson Vincent , Annesa Flentje , Benjamin S. Dominguez , Robert H. Paul , Savita Pahwa , Suresh Pallikkuth , Margaret Roach , Dietmar Fuchs , Samantha E. Dilworth , Torsten B. Neilands , Peter W. Hunt , Gowri Sunder , Cody Lentz , Sydney Telaak , Adam W. Carrico","doi":"10.1016/j.bbih.2025.101156","DOIUrl":"10.1016/j.bbih.2025.101156","url":null,"abstract":"<div><h3>Background</h3><div>Microbial translocation, immune activation, inflammation, and dysregulated metabolism of neurotransmitter precursors are interacting pathophysiologic processes linked to neuropsychiatric comorbidities and faster HIV disease progression. We examined correlates of distinct phenotypes of gut-immune dysregulation in people living with HIV (PWH) who use methamphetamine.</div></div><div><h3>Methods</h3><div>Participants were 122 PWH who had biochemically confirmed recent methamphetamine use, including non-injection use. Peripheral plasma markers reflected: intestinal permeability, microbial translocation, immune activation, inflammation, and dysregulated metabolism of neurotransmitter precursors. Using latent profile analysis (i.e., clustering) of these markers, we identified gut-immune phenotypes and their clinical, demographic, and stigma-related correlates.</div></div><div><h3>Results</h3><div>Three immune profiles emerged: (1) <em>low gut-immune dysregulation</em> with lower microbial translocation, macrophage activation, inflammation, and tryptophan catabolism; (2) <em>moderate gut-immune dysregulation</em> with all markers within average range; and (3) <em>high gut-immune dysregulation</em> with higher microbial translocation, immune activation, inflammation, and tryptophan catabolism. In adjusted analyses, higher viral load (one log10 copy/ml; <em>AOR</em> = 1.97, 95 % CI = 1.02–3.82), injection of methamphetamine (<em>AOR</em> = 3.60, 95 % CI = 1.23–10.50), and internalized stigma (<em>AOR</em> = 1.78, 95 % CI = 1.01–3.15) were associated with having a moderate gut-immune dysregulation profile. Additionally, higher viral load (<em>AOR</em> = 2.98, 95 % CI = 1.53–5.24) and injecting methamphetamine (<em>AOR</em> = 5.45, 95 % CI = 1.34–17.78) were associated with having a high gut-immune dysregulation profile.</div></div><div><h3>Conclusions</h3><div>Distinct patterns of microbial translocation, immune activation, inflammation, and metabolism of amino acid precursors distinguished gut-immune phenotypes of PWH reporting injection methamphetamine use and greater internalized stigma. Interventions tailored to PWH who inject methamphetamine or struggle with internalized stigma could optimize HIV-related health outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101156"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712257","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}
Pub Date : 2026-02-01Epub Date: 2025-12-18DOI: 10.1016/j.bbih.2025.101163
Faith Dickerson , Emily Katsafanas , Andrea Origoni , Kelly Rowe , Sabahat Khan , Fahad Mukhtar , Shuojja Yang , Victor W. Splan , Robert Yolken
Matrix metalloproteinases (MMPs) are a diverse set of enzymes associated with tissue remodeling as well as inflammation and tissue destruction. MMP-9 is of interest since it has been associated with psychiatric disorders including major depressive disorder (MDD). Suicide attempts are a major complication of MDD. However, the association between MMP-9 levels and suicide attempts has not been extensively studied in persons with MDD. Sensitive enzyme immunoassays were employed to measure the levels of MMP-9 in blood samples from 186 persons with MDD receiving hospital care, 92 with a suicide attempt within the previous 30 days and 94 without a recent attempt, as well as 79 persons without a psychiatric disorder. Lifetime suicide attempt history in the MDD group was also recorded. Mixed effects models were employed to compare the MMP-9 levels among the groups adjusted for demographic and clinical variables. Wald tests were used to calculate pairwise comparisons. Employing these models, we found that individuals with MDD and a recent suicide attempt had higher levels of MMP-9 than individuals with MDD without a recent suicide attempt as well as individuals without a psychiatric disorder. There was not a significant difference in MMP-9 levels between the non-psychiatric group and individuals with MDD without a recent suicide attempt, regardless of whether they had a lifetime suicide attempt. Therapeutic modalities to modulate MMP-9 activity are currently being developed. The measurement of MMP-9 might be used to inform future clinical trials of these modalities for the prevention of suicide behaviors in high-risk individuals.
{"title":"Levels of matrix metalloproteinase 9 (MMP-9) are elevated in persons with major depressive disorder who have had a recent suicide attempt","authors":"Faith Dickerson , Emily Katsafanas , Andrea Origoni , Kelly Rowe , Sabahat Khan , Fahad Mukhtar , Shuojja Yang , Victor W. Splan , Robert Yolken","doi":"10.1016/j.bbih.2025.101163","DOIUrl":"10.1016/j.bbih.2025.101163","url":null,"abstract":"<div><div>Matrix metalloproteinases (MMPs) are a diverse set of enzymes associated with tissue remodeling as well as inflammation and tissue destruction. MMP-9 is of interest since it has been associated with psychiatric disorders including major depressive disorder (MDD). Suicide attempts are a major complication of MDD. However, the association between MMP-9 levels and suicide attempts has not been extensively studied in persons with MDD. Sensitive enzyme immunoassays were employed to measure the levels of MMP-9 in blood samples from 186 persons with MDD receiving hospital care, 92 with a suicide attempt within the previous 30 days and 94 without a recent attempt, as well as 79 persons without a psychiatric disorder. Lifetime suicide attempt history in the MDD group was also recorded. Mixed effects models were employed to compare the MMP-9 levels among the groups adjusted for demographic and clinical variables. Wald tests were used to calculate pairwise comparisons. Employing these models, we found that individuals with MDD and a recent suicide attempt had higher levels of MMP-9 than individuals with MDD without a recent suicide attempt as well as individuals without a psychiatric disorder. There was not a significant difference in MMP-9 levels between the non-psychiatric group and individuals with MDD without a recent suicide attempt, regardless of whether they had a lifetime suicide attempt. Therapeutic modalities to modulate MMP-9 activity are currently being developed. The measurement of MMP-9 might be used to inform future clinical trials of these modalities for the prevention of suicide behaviors in high-risk individuals.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101163"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939224","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}
Pub Date : 2026-02-01Epub Date: 2025-12-30DOI: 10.1016/j.bbih.2025.101167
Chun-Ling Dai , Yiting Song , Yonghua Chen , Yunn Chyn Tung , Wei-Chiao Huang , Cheng-Xin Gong , Jonathan F. Lovell
Amyloid beta (Aβ) plaques and hyperphosphorylated tau neurofibrillary tangles (NFTs) are the histopathological hallmarks of Alzheimer's disease (AD) and targets for AD therapeutics. Since Aβ and tau pathologies both drive AD pathogenesis and progression, immunotherapies singularly targeting either Aβ or tau may be limited, and simultaneously targeting multiple epitopes of both Aβ and tau may be an efficacious approach. We developed a novel vaccine including three his-tagged tau peptides, tau1-22, mid-region tau171-191 (taupT181), and tau388-407 (taupS396/S404), as well as two his-tagged Aβ fragments (N-terminal Aβ1-14 and N-terminal pyroglutamate AβpE3-14) with the spontaneous nanoliposome antigen particle (SNAP) system, termed SNAP-AD5. Intramuscular vaccination of nine to ten months old of 3xTg-AD mice and age-matched wild-type control animals with SNAP-AD5 or adjuvant only, once every three weeks for a total of 5 immunizations, simultaneously produced IgG titers of antibody against their specific antigens, significantly decreased Aβ and tau pathologies, and effectively improved cognitive function. SNAP-AD5 was well tolerated without any detectable adverse side effects, including inflammatory responses in the peripheral circulation and in the brain, and hemorrhages in the mouse brain. These results support that SNAP-AD5 simultaneously targeting both Aβ and tau is potentially a promising new approach for treating AD. Further optimization and development of the SNAP-AD5 vaccine for treating AD is warranted.
{"title":"Therapeutic nanoliposome vaccine targeting multiple Aβ and tau epitopes reduces AD-like brain pathologies and rescues cognitive deficits in 3xTg-AD mice","authors":"Chun-Ling Dai , Yiting Song , Yonghua Chen , Yunn Chyn Tung , Wei-Chiao Huang , Cheng-Xin Gong , Jonathan F. Lovell","doi":"10.1016/j.bbih.2025.101167","DOIUrl":"10.1016/j.bbih.2025.101167","url":null,"abstract":"<div><div>Amyloid beta (Aβ) plaques and hyperphosphorylated tau neurofibrillary tangles (NFTs) are the histopathological hallmarks of Alzheimer's disease (AD) and targets for AD therapeutics. Since Aβ and tau pathologies both drive AD pathogenesis and progression, immunotherapies singularly targeting either Aβ or tau may be limited, and simultaneously targeting multiple epitopes of both Aβ and tau may be an efficacious approach. We developed a novel vaccine including three his-tagged tau peptides, tau<sub>1-22</sub>, mid-region tau<sub>171-191</sub> (tau<sub>pT181</sub>), and tau<sub>388-407</sub> (tau<sub>pS396/S404</sub>), as well as two his-tagged Aβ fragments (N-terminal Aβ<sub>1-14</sub> and N-terminal pyroglutamate Aβ<sub>pE3-14</sub>) with the spontaneous nanoliposome antigen particle (SNAP) system, termed SNAP-AD<sub>5</sub>. Intramuscular vaccination of nine to ten months old of 3xTg-AD mice and age-matched wild-type control animals with SNAP-AD<sub>5</sub> or adjuvant only, once every three weeks for a total of 5 immunizations, simultaneously produced IgG titers of antibody against their specific antigens, significantly decreased Aβ and tau pathologies, and effectively improved cognitive function. SNAP-AD<sub>5</sub> was well tolerated without any detectable adverse side effects, including inflammatory responses in the peripheral circulation and in the brain, and hemorrhages in the mouse brain. These results support that SNAP-AD<sub>5</sub> simultaneously targeting both Aβ and tau is potentially a promising new approach for treating AD. Further optimization and development of the SNAP-AD<sub>5</sub> vaccine for treating AD is warranted.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101167"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939125","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}
Pub Date : 2026-02-01Epub Date: 2025-12-22DOI: 10.1016/j.bbih.2025.101162
Bengt B. Arnetz , Judith E. Arnetz , Norbert Kaminski , Ryan Tomlin , Pamela Bartlett , Robert Crawford , Andrew Jameson
Background
There is limited description of dynamic changes in stress, inflammation, neuroplasticity, and health literacy during the early phase of HIV infection. This study examined patterns in self-reported stress, neurobiological and neuroplastic markers during the initial 12 months of living with HIV. The study also evaluated possible changes in functional health literacy, that is, patients’ ability to adhere to combination antiretroviral treatment (cART).
Methods
This is an observational cohort study of one female and eleven male and patients with newly diagnosed HIV attending an urban Ryan White funded HIV clinic. Participants responded to a survey and blood was drawn at baseline, and after 1, 3, 6, 9 and 12 months, respectively. The survey measured stress, depression, and health literacy. Blood was analyzed for HIV RNA plasma viral load, CD4 cell count, and biomarkers of stress, inflammation, and neuroplasticity.
Results
Viral load decreased from an initial mean count of 353,714.83 (S.E. 251,243.96) copies/mL to 24.54 (2.01) at 12 months (Wilcoxon Signed Rank Test, p = .012). CD4 cell count increased from 321.08 (48.49) to 541.13 (50.27) cells/mm3 (p = .012). Self-rated stress decreased from 6.83 (.92) to 4.81 (.96), on a 0–10 visual analogue scale (p = .043). Cumulative levels of C-reactive protein (CRP) were inversely associated with cumulative health literacy scores during the 12-month study (Spearman's rho = - 0.634, p = .025).
Conclusion
The study confirms that during the initial 12 months living with HIV, apart from the expected improvement in viral load and CD4, there is a significant decrease in self-perceived stress, but little changes in systems inflammation. The finding of an inverse relationship between levels of a pro-inflammatory marker and health literacy requires further studies.
{"title":"Self-reported health and health literacy, neuroplasticity and neuro-immunological markers during the first 12 months in newly diagnosed people living with HIV: An exploratory study","authors":"Bengt B. Arnetz , Judith E. Arnetz , Norbert Kaminski , Ryan Tomlin , Pamela Bartlett , Robert Crawford , Andrew Jameson","doi":"10.1016/j.bbih.2025.101162","DOIUrl":"10.1016/j.bbih.2025.101162","url":null,"abstract":"<div><h3>Background</h3><div>There is limited description of dynamic changes in stress, inflammation, neuroplasticity, and health literacy during the early phase of HIV infection. This study examined patterns in self-reported stress, neurobiological and neuroplastic markers during the initial 12 months of living with HIV. The study also evaluated possible changes in functional health literacy, that is, patients’ ability to adhere to combination antiretroviral treatment (cART).</div></div><div><h3>Methods</h3><div>This is an observational cohort study of one female and eleven male and patients with newly diagnosed HIV attending an urban Ryan White funded HIV clinic. Participants responded to a survey and blood was drawn at baseline, and after 1, 3, 6, 9 and 12 months, respectively. The survey measured stress, depression, and health literacy. Blood was analyzed for HIV RNA plasma viral load, CD4 cell count, and biomarkers of stress, inflammation, and neuroplasticity.</div></div><div><h3>Results</h3><div>Viral load decreased from an initial mean count of 353,714.83 (S.E. 251,243.96) copies/mL to 24.54 (2.01) at 12 months (Wilcoxon Signed Rank Test, p = .012). CD4 cell count increased from 321.08 (48.49) to 541.13 (50.27) cells/mm<sup>3</sup> (p = .012). Self-rated stress decreased from 6.83 (.92) to 4.81 (.96), on a 0–10 visual analogue scale (p = .043). Cumulative levels of C-reactive protein (CRP) were inversely associated with cumulative health literacy scores during the 12-month study (Spearman's rho = - 0.634, p = .025).</div></div><div><h3>Conclusion</h3><div>The study confirms that during the initial 12 months living with HIV, apart from the expected improvement in viral load and CD4, there is a significant decrease in self-perceived stress, but little changes in systems inflammation. The finding of an inverse relationship between levels of a pro-inflammatory marker and health literacy requires further studies.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101162"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939124","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}
Pub Date : 2026-02-01Epub Date: 2025-12-18DOI: 10.1016/j.bbih.2025.101161
Weiye Chen, Ian N. Johnston
A subset of cancer patients and survivors experience cognitive decline during and after chemotherapy, a condition known as chemotherapy-induced cognitive impairment (CICI). Among the most affected domains are executive functions (EFs) - a set of higher-order cognitive processes essential for goal-directed behaviour, including working memory, behavioural flexibility, and inhibition. Emerging evidence suggests that these domains are differentially susceptible to chemotherapy drugs, implicating the selective disruption of distinct neural circuits and neurochemical pathways. To better understand the underlying mechanisms, we conducted a systematic review of rodent models of CICI, focusing on neurobiological alterations associated with chemotherapy and their relationship to EF deficits. A comprehensive search across PubMed, Web of Science, Scopus, and PsycINFO identified 67 eligible papers. Across studies, working memory and problem-solving impairments were most frequently examined and showed the greatest overlap across multiple mechanistic categories, including oxidative stress, mitochondrial dysfunction, neuroimmune dysregulation, impaired plasticity, and altered white matter integrity. Behavioural flexibility was most often linked to disrupted neurogenesis and metabolic imbalance, whereas attention and inhibition showed variable associations with neurotransmission and synaptic markers. Considerable heterogeneity within mechanistic categories reflected interactions among treatment regimen, animal sex, strain, and timing of assessment. Future studies should integrate molecular, cellular, and systems-level analyses within longitudinal and sex-balanced designs to clarify causal mechanisms and guide targeted interventions for preserving cognitive health in cancer survivors.
一部分癌症患者和幸存者在化疗期间和之后经历认知能力下降，这种情况被称为化疗诱导的认知障碍（CICI）。其中受影响最大的领域是执行功能（EFs），这是一组对目标导向行为至关重要的高阶认知过程，包括工作记忆、行为灵活性和抑制。新出现的证据表明，这些区域对化疗药物的敏感性不同，这意味着不同的神经回路和神经化学途径的选择性破坏。为了更好地了解潜在的机制，我们对CICI的啮齿动物模型进行了系统的回顾，重点关注与化疗相关的神经生物学改变及其与EF缺陷的关系。在PubMed， Web of Science， Scopus和PsycINFO上进行全面搜索，确定了67篇符合条件的论文。在所有研究中，工作记忆和解决问题的障碍是最常被检查的，并且在多个机制类别中显示出最大的重叠，包括氧化应激、线粒体功能障碍、神经免疫失调、可塑性受损和白质完整性改变。行为灵活性通常与神经发生紊乱和代谢失衡有关，而注意力和抑制则与神经传递和突触标志物有不同的关联。机制分类中相当大的异质性反映了治疗方案、动物性别、品系和评估时间之间的相互作用。未来的研究应该在纵向和性别平衡设计中整合分子、细胞和系统水平的分析，以阐明因果机制，并指导有针对性的干预措施，以保持癌症幸存者的认知健康。
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Pub Date : 2026-02-01Epub Date: 2025-12-22DOI: 10.1016/j.bbih.2025.101165
Elise M. Martin, Matthew J. Morales, Niki Y. Li, Maura C. Stoehr, Matthew J. Kern, Madeline F. Winters, Caroline J. Smith
Air pollution and maternal stress during pregnancy are both risk factors for neurodevelopmental disorders and often converge on the same communities. Epidemiological and animal studies suggest that maternal psychosocial stress may worsen the effects of air pollutants on neurodevelopmental outcomes. Previous work utilizing a mouse model of combined prenatal exposure to diesel exhaust particles (DEP) and maternal stress (MS) has found numerous sex-specific effects of DEP/MS exposure on neuroimmune outcomes, dopamine receptors, the gut-brain axis, and social behavior. However, it is unclear how broadly the immune landscape is shifted in the brain and intestinal epithelium following DEP/MS. Here, we analyzed immune gene expression in 5 brain regions important for social behavior and in 3 regions of the intestinal epithelium in both male and female offspring at ∼postnatal day 50, following either DEP/MS or control exposure. We found several interesting overall patterns. First, changes in expression of immune genes such as CD11b and Tlr4 were concentrated in the nucleus accumbens and hippocampus. Tlr4 and Il-17ra mRNA also increased in the jejunum and colon following DEP/MS, but only in females. Second, in the nucleus accumbens, catecholamine-O-methyltransferase (Comt) and dopamine transporter 1 (Slc6a3) gene expression were increased following DEP/MS, indicating increased dopamine degradation at and reuptake from the synapse, respectively. Additionally, dopamine D2 receptor (Drd2) mRNA was decreased following DEP/MS in males. Finally, we observed numerous sex differences in immune gene expression regardless of treatment in both the brain and gut. Together, these findings suggest the nucleus accumbens is a key site for neuroimmune and dopaminergic changes following DEP/MS exposure and indicate female-specific changes in intestinal immunity in young adulthood following these prenatal exposures.
空气污染和怀孕期间的产妇压力都是神经发育障碍的危险因素，而且往往集中在同一社区。流行病学和动物研究表明，母亲的社会心理压力可能会加重空气污染物对神经发育结果的影响。先前的研究利用了一个小鼠模型，将产前暴露于柴油机尾气颗粒（DEP）和母亲压力（MS）相结合，发现了DEP/MS暴露对神经免疫结果、多巴胺受体、肠-脑轴和社会行为的许多性别特异性影响。然而，目前尚不清楚DEP/MS后脑和肠上皮的免疫格局发生了多大程度的变化。在这里，我们分析了DEP/MS或对照暴露后，出生后第50天雄性和雌性后代在5个对社会行为重要的大脑区域和3个肠上皮区域的免疫基因表达。我们发现了几个有趣的总体模式。首先，CD11b、Tlr4等免疫基因的表达变化集中在伏隔核和海马。在DEP/MS后，空肠和结肠的Tlr4和Il-17ra mRNA也增加，但仅在女性中增加。其次，在伏隔核中，DEP/MS后，儿茶酚胺- o -甲基转移酶（Comt）和多巴胺转运蛋白1 （Slc6a3）基因表达增加，分别表明突触的多巴胺降解和从突触的再摄取增加。此外，DEP/MS后，雄性多巴胺D2受体（Drd2） mRNA降低。最后，无论在大脑和肠道中接受何种治疗，我们都观察到免疫基因表达的许多性别差异。总之，这些发现表明伏隔核是DEP/MS暴露后神经免疫和多巴胺能变化的关键部位，并表明这些产前暴露后年轻成年期肠道免疫的女性特异性变化。
{"title":"Effects of combined prenatal exposure to air pollution and maternal stress on immune and dopaminergic gene expression in the gut-brain axis","authors":"Elise M. Martin, Matthew J. Morales, Niki Y. Li, Maura C. Stoehr, Matthew J. Kern, Madeline F. Winters, Caroline J. Smith","doi":"10.1016/j.bbih.2025.101165","DOIUrl":"10.1016/j.bbih.2025.101165","url":null,"abstract":"<div><div>Air pollution and maternal stress during pregnancy are both risk factors for neurodevelopmental disorders and often converge on the same communities. Epidemiological and animal studies suggest that maternal psychosocial stress may worsen the effects of air pollutants on neurodevelopmental outcomes. Previous work utilizing a mouse model of combined prenatal exposure to diesel exhaust particles (DEP) and maternal stress (MS) has found numerous sex-specific effects of DEP/MS exposure on neuroimmune outcomes, dopamine receptors, the gut-brain axis, and social behavior. However, it is unclear how broadly the immune landscape is shifted in the brain and intestinal epithelium following DEP/MS. Here, we analyzed immune gene expression in 5 brain regions important for social behavior and in 3 regions of the intestinal epithelium in both male and female offspring at ∼postnatal day 50, following either DEP/MS or control exposure. We found several interesting overall patterns. First, changes in expression of immune genes such as <em>CD11b</em> and <em>Tlr4</em> were concentrated in the nucleus accumbens and hippocampus. <em>Tlr4</em> and <em>Il-17ra</em> mRNA also increased in the jejunum and colon following DEP/MS, but only in females. Second, in the nucleus accumbens, catecholamine-O-methyltransferase (<em>Comt</em>) and dopamine transporter 1 (<em>Slc6a3</em>) gene expression were increased following DEP/MS, indicating increased dopamine degradation at and reuptake from the synapse, respectively. Additionally, dopamine D2 receptor (<em>Drd2</em>) mRNA was decreased following DEP/MS in males. Finally, we observed numerous sex differences in immune gene expression regardless of treatment in both the brain and gut. Together, these findings suggest the nucleus accumbens is a key site for neuroimmune and dopaminergic changes following DEP/MS exposure and indicate female-specific changes in intestinal immunity in young adulthood following these prenatal exposures.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101165"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939222","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}
Psychological distress (depression, anxiety, stress) is common in inflammatory bowel disease (IBD) and is linked to poorer outcomes, yet behavioural pathways and economic consequences remain unclear. This study tested a gut-brain-behaviour-outcome (GBBO) framework, testing: 1) reciprocal links between distress and disease activity; 2) whether health behaviours mediate distress-disease activity relationships; 3) if distress and self-reported disease activity (SRDA) predict adverse disease outcomes, controlling for inflammation and 4) whether disease activity mediates relationships between distress and adverse outcomes.
Methods
IBD patients (n = 157) reported distress, health behaviours, SRDA, healthcare use and disease-related outcomes at 3 waves at 6-month intervals. Faecal calprotectin (FCP) was assayed at baseline and 6 months. Analyses were conducted using structural equation modelling and mixed-effects models.
Results
Baseline distress predicted higher SRDA six months later (β = 0.16, p=.03) but did not predict FCP; reverse pathways were nonsignificant. Impaired sleep quality mediated 55 % of the effect of distress on future SRDA (β = 0.09, p=.04). Other behaviours were nonsignificant. Controlling for FCP, distress and SRDA independently predicted secondary healthcare usage (primary/secondary care) and disease-related outcomes (flare frequency/severity, absenteeism and productivity loss). FCP was positively related to flare frequency/severity and allied health practitioner visits only. Mediation analysis showed that SRDA partially mediated absenteeism.
Conclusions
Psychological distress exacerbates symptoms and economic cost. Poor sleep partially mediates the relationship between distress and SRDA, but not inflammation. Psychological interventions that focus on improving sleep could be cost-effective ways to improve mental health and symptom burden, with downstream impact on healthcare utilisation and productivity losses.
{"title":"Psychological distress predicts disease activity in inflammatory bowel disease: Results from the mind-body IBD longitudinal study","authors":"Natasha Seaton , Joanna L. Hudson , Valeria Mondelli , Leah Raymond , Pooja Schmill , Ailsa Hart , Rona Moss-Morris","doi":"10.1016/j.bbih.2025.101147","DOIUrl":"10.1016/j.bbih.2025.101147","url":null,"abstract":"<div><h3>Background & aims</h3><div>Psychological distress (depression, anxiety, stress) is common in inflammatory bowel disease (IBD) and is linked to poorer outcomes, yet behavioural pathways and economic consequences remain unclear. This study tested a gut-brain-behaviour-outcome (GBBO) framework, testing: 1) reciprocal links between distress and disease activity; 2) whether health behaviours mediate distress-disease activity relationships; 3) if distress and self-reported disease activity (SRDA) predict adverse disease outcomes, controlling for inflammation and 4) whether disease activity mediates relationships between distress and adverse outcomes.</div></div><div><h3>Methods</h3><div>IBD patients (n = 157) reported distress, health behaviours, SRDA, healthcare use and disease-related outcomes at 3 waves at 6-month intervals. Faecal calprotectin (FCP) was assayed at baseline and 6 months. Analyses were conducted using structural equation modelling and mixed-effects models.</div></div><div><h3>Results</h3><div>Baseline distress predicted higher SRDA six months later (β = 0.16, <em>p=.</em>03) but did not predict FCP; reverse pathways were nonsignificant. Impaired sleep quality mediated 55 % of the effect of distress on future SRDA (β = 0.09, <em>p=.</em>04). Other behaviours were nonsignificant. Controlling for FCP, distress and SRDA independently predicted secondary healthcare usage (primary/secondary care) and disease-related outcomes (flare frequency/severity, absenteeism and productivity loss). FCP was positively related to flare frequency/severity and allied health practitioner visits only. Mediation analysis showed that SRDA partially mediated absenteeism.</div></div><div><h3>Conclusions</h3><div>Psychological distress exacerbates symptoms and economic cost. Poor sleep partially mediates the relationship between distress and SRDA, but not inflammation. Psychological interventions that focus on improving sleep could be cost-effective ways to improve mental health and symptom burden, with downstream impact on healthcare utilisation and productivity losses.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101147"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746985","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}
Pub Date : 2025-12-01Epub Date: 2025-11-25DOI: 10.1016/j.bbih.2025.101146
Alicia J. Smith , Stacey Kigar , Quentin Dercon , Mary-Ellen Lynall , Konstantinos Ioannidis , Muzaffer Kaser , Caitlin Hitchcock , Tim Dalgleish , Camilla L. Nord
<div><h3>Background</h3><div>Psychiatric disorders are increasingly conceptualised as heterogeneous categories with transdiagnostic underlying mechanisms that cut across multiple diagnoses and vary within a single diagnosis. Inflammation induced by psychosocial stress is one particularly potent example: previous research suggests that inflammatory profiles may correspond to symptom subgroups rather than traditional diagnostic categories. However, robust identification of transdiagnostic symptoms linked to specific inflammatory profiles remains rare. In this study, we examined the relationship between inflammatory profiles (at baseline and after a stress induction) and transdiagnostic symptom dimensions in females, who show higher prevalence of stress-related disorders such as anxiety and depression.</div></div><div><h3>Methods</h3><div>A modest but relatively homogenous healthy female sample, between the ages of 18 and 35, was recruited (N = 26). We obtained venous blood samples, at baseline and after a combined physiological and social stress induction, to measure full blood counts, plasma cytokines and peripheral blood mononuclear cells (PBMCs; for cell stimulation and intracellular flow cytometry analysis). Participants completed a battery of psychiatric self-report questions, from which we modelled three transdiagnostic factor scores. Finally, we used Bayesian regressions to evaluate the predictive contribution of transdiagnostic factors to inflammatory markers (at baseline and stress-induced), as well as to the principal components of inflammatory measures (derived from a principal component analysis (PCA) of the inflammatory data).</div></div><div><h3>Results</h3><div>We identified specific relationships between inflammatory profiles and transdiagnostic symptom dimensions. Higher scores on a ‘social withdrawal’ factor were associated with greater baseline neutrophil (95 % highest density interval (HDI) = [0.06, 1.32]; BF<sub>10</sub> = 2.92) and monocyte counts (95 % HDI = [0.29, 1.46]; BF<sub>10</sub> = 19.08), whereas higher ‘anxious-depression’ scores were associated with a lower baseline monocyte count (95 % HDI = [-0.96, −0.02]; BF<sub>10</sub> = 1.81) and a greater inflammatory response to stress (e.g., change in neutrophil scores from pre-to post stress induction: (95 % HDI = [0.18, 2.14]); BF<sub>10</sub> = 5.66). We also found evidence for an association between the ‘social withdrawal’ factor and an immune principal component most strongly weighted by monocytes, basophils, and IL-6 (95 % HDI = [-1.14, −0.01]; BF<sub>10</sub> = 1.88).</div></div><div><h3>Conclusions</h3><div>We find preliminary evidence that different transdiagnostic psychiatric symptom dimensions map onto specific inflammatory profiles, both at baseline and after a stress induction. This represents a proof-of-principle for the use of data-driven and hypothesis-driven approaches to identify and link transdiagnostic factors with inflammatory changes, which may be of
{"title":"Inflammatory profiles of transdiagnostic symptom dimensions in healthy females","authors":"Alicia J. Smith , Stacey Kigar , Quentin Dercon , Mary-Ellen Lynall , Konstantinos Ioannidis , Muzaffer Kaser , Caitlin Hitchcock , Tim Dalgleish , Camilla L. Nord","doi":"10.1016/j.bbih.2025.101146","DOIUrl":"10.1016/j.bbih.2025.101146","url":null,"abstract":"<div><h3>Background</h3><div>Psychiatric disorders are increasingly conceptualised as heterogeneous categories with transdiagnostic underlying mechanisms that cut across multiple diagnoses and vary within a single diagnosis. Inflammation induced by psychosocial stress is one particularly potent example: previous research suggests that inflammatory profiles may correspond to symptom subgroups rather than traditional diagnostic categories. However, robust identification of transdiagnostic symptoms linked to specific inflammatory profiles remains rare. In this study, we examined the relationship between inflammatory profiles (at baseline and after a stress induction) and transdiagnostic symptom dimensions in females, who show higher prevalence of stress-related disorders such as anxiety and depression.</div></div><div><h3>Methods</h3><div>A modest but relatively homogenous healthy female sample, between the ages of 18 and 35, was recruited (N = 26). We obtained venous blood samples, at baseline and after a combined physiological and social stress induction, to measure full blood counts, plasma cytokines and peripheral blood mononuclear cells (PBMCs; for cell stimulation and intracellular flow cytometry analysis). Participants completed a battery of psychiatric self-report questions, from which we modelled three transdiagnostic factor scores. Finally, we used Bayesian regressions to evaluate the predictive contribution of transdiagnostic factors to inflammatory markers (at baseline and stress-induced), as well as to the principal components of inflammatory measures (derived from a principal component analysis (PCA) of the inflammatory data).</div></div><div><h3>Results</h3><div>We identified specific relationships between inflammatory profiles and transdiagnostic symptom dimensions. Higher scores on a ‘social withdrawal’ factor were associated with greater baseline neutrophil (95 % highest density interval (HDI) = [0.06, 1.32]; BF<sub>10</sub> = 2.92) and monocyte counts (95 % HDI = [0.29, 1.46]; BF<sub>10</sub> = 19.08), whereas higher ‘anxious-depression’ scores were associated with a lower baseline monocyte count (95 % HDI = [-0.96, −0.02]; BF<sub>10</sub> = 1.81) and a greater inflammatory response to stress (e.g., change in neutrophil scores from pre-to post stress induction: (95 % HDI = [0.18, 2.14]); BF<sub>10</sub> = 5.66). We also found evidence for an association between the ‘social withdrawal’ factor and an immune principal component most strongly weighted by monocytes, basophils, and IL-6 (95 % HDI = [-1.14, −0.01]; BF<sub>10</sub> = 1.88).</div></div><div><h3>Conclusions</h3><div>We find preliminary evidence that different transdiagnostic psychiatric symptom dimensions map onto specific inflammatory profiles, both at baseline and after a stress induction. This represents a proof-of-principle for the use of data-driven and hypothesis-driven approaches to identify and link transdiagnostic factors with inflammatory changes, which may be of ","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"50 ","pages":"Article 101146"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684162","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}
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