Brain, behavior, & immunity - health最新文献

{"title":"Specific immune-inflammatory profiles and neurocognitive deficits predict illness trajectories in people with type 2 diabetes mellitus or psychiatric disorders","authors":"Joan Vicent Sánchez-Ortí , Patricia Correa-Ghisays , Vicent Balanzá-Martínez , Gabriel Selva-Vera , Víctor M. Victor , Constanza San Martin Valenzuela , Pau Soldevila-Matías , Fabián Robledo-Yagüe , María Flores-Rodero , Jon Sánchez-Valle , Jaume Forés-Martos , Diego Macías Saint-Gerons , Inmaculada Fuentes-Durá , Rafael Tabarés-Seisdedos","doi":"10.1016/j.bbih.2025.100962","DOIUrl":"10.1016/j.bbih.2025.100962","url":null,"abstract":"<div><h3>Introduction</h3><div>Psychiatric disorders and type 2 diabetes mellitus (T2DM) are chronic conditions that are often comorbid with each other. Neurocognitive and functional impairments are associated with numerous clinical changes during the course of illness. Immune-inflammatory dysfunction is emerging as a critical factor in the progression of these disorders. This study aimed to identify neurocognitive deficits and immune-inflammatory biomarkers that are suitable for signaling different illness trajectories from transdiagnostic and longitudinal perspectives.</div></div><div><h3>Methods</h3><div>Clinical status, neurocognitive and functional performance, and peripheral blood biomarkers of immune-inflammation were assessed twice a year in 165 individuals, including 30 with schizophrenia (SZ), 42 with bipolar disorder (BD), 35 with major depressive disorder (MDD), 30 with T2DM, and 28 healthy controls (HCs). Participants with chronic illness (n = 137) were stratified into quartiles, taking their years of illness duration at baseline as a reference into categories of short illness duration (SD; n = 37), middle illness duration (MD; n = 36), long illness duration (LD; n = 32), and very long illness duration (VLD; n = 32). The illness duration was used to measure the illness trajectory, and the exposure of interest was clinical progression, calculated as the difference between clinical severity at baseline (T1) and after 1 year (T2).</div></div><div><h3>Results</h3><div>Neurocognitive impairment was more significant in the VLD group than in the other groups, with small–moderate effect sizes (F = 2.9 to 9.3; p < 0.05−0.0001; η<sup>2</sup>p = 0.06−0.24). Moreover, the HC group showed significantly higher functional outcomes than the other groups (F = 5.8 to 6.0; p < 0.0001; η<sup>2</sup>p = 0.13−0.16). On the contrary, the HC group showed lower levels of immune-inflammatory markers (white blood cell count, absolute neutrophils, absolute monocytes, absolute basophiles, neutrophils/lymphocyte ratio, and platelets/lymphocyte ratio [PLR]) (F = 2.9 to 6.7; p < 0.05−0.0001; η<sup>2</sup>p = 0.07−0.18). In all groups, significant prospective associations were observed between cognitive function (short-term memory and processing speed), global functional scores, immune-inflammatory biomarkers (monocyte/lymphocyte ratio [MLR] and PLR), and clinical status (p < 0.05). Furthermore, a similar combination of neurocognitive deficits and immune-inflammatory alterations compounded the transdiagnostic model that best discriminated the different illness trajectories (χ<sup>2</sup> = 67.4 to 78.7; p < 0.05−0.01).</div></div><div><h3>Conclusions</h3><div>Neurocognitive dysfunction and systemic inflammation are associated with prolonged illness trajectories in individuals with psychiatric disorders and T2DM. An immune-inflammatory profile and neurocognitive and functional performance may be valuable to differentiate individuals with different illn","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100962"},"PeriodicalIF":3.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The vagus nerve-dependent lung-brain axis mediates brain demyelination following acute lung injury","authors":"Dan Xu ,&nbsp;Mingming Zhao ,&nbsp;Guilin Liu ,&nbsp;Tingting Zhu ,&nbsp;Yi Cai ,&nbsp;Rumi Murayama ,&nbsp;Yong Yue ,&nbsp;Kenji Hashimoto","doi":"10.1016/j.bbih.2025.100966","DOIUrl":"10.1016/j.bbih.2025.100966","url":null,"abstract":"<div><div>Patients with acute lung injury (ALI) often experience psychiatric and neurological symptoms; however, the precise underlying mechanisms remain unclear. Given that white matter loss (demyelination) contributes to these symptoms, we investigated whether lipopolysaccharide (LPS)-induced ALI leads to brain demyelination via a vagus nerve-dependent lung-brain axis. A single intratracheal injection of LPS caused severe lung injury and demyelination in the corpus callosum (CC) of mouse brains. Subdiaphragmatic vagotomy did not affect LPS-induced lung injury or demyelination in the CC. Interestingly, cervical vagotomy significantly attenuated LPS-induced hypo-locomotion, plasma interleukin-6 levels, and demyelination in the CC of ALI mice without influencing lung injury. These findings demonstrate that ALI can induce demyelination in the CC of the mouse brain via a cervical vagus nerve-dependent lung-brain axis, highlighting the critical role of this pathway in the psychiatric and neurological symptoms observed in ALI patients.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100966"},"PeriodicalIF":3.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preliminary evaluation of a mindfulness intervention program in women with long COVID dysautonomia symptoms","authors":"Elizabeth Vandenbogaart ,&nbsp;Matthew Figueroa ,&nbsp;Diana Winston ,&nbsp;Steve Cole ,&nbsp;Julienne Bower ,&nbsp;Jeffrey J. Hsu","doi":"10.1016/j.bbih.2025.100963","DOIUrl":"10.1016/j.bbih.2025.100963","url":null,"abstract":"<div><h3>Background</h3><div>The symptom burden for patients with Long COVID-associated dysautonomia is high, yet there are currently no effective treatments. Mindfulness programs reduce psychological and physical symptoms as well as inflammatory gene expression in a variety of medical conditions. The study aim was to evaluate the effect of a six-week mindfulness program in women with Long COVID dysautonomia symptoms.</div></div><div><h3>Methods</h3><div>Using a single arm, pre- and posttest design, women aged 18–54 years with Long COVID and orthostatic intolerance suggestive of dysautonomia were recruited from a single center. Participants attended a standardized, six-week, virtual mindfulness program. An active stand test and 6-min walk test (6MWT) were performed at baseline and post-intervention. Self-reported measures of physical and mental health symptoms collected at baseline, post-intervention and 4 week follow up included the composite autonomic symptom score (COMPASS-31), perceived stress (PSS), anxiety (GAD7), depression (PHQ8), COVID-19 event specific distress (IES-R), fatigue (FSI), sleep (ISI), well-being (MHC-SF), resilience (CD-RISC 10), and quality of life (SF-20). The effects on conserved transcriptional response to adversity (CTRA) were examined by next-generation sequencing of dried whole blood samples.</div></div><div><h3>Results</h3><div>Twenty participants were enrolled with a mean age of 39.9 years (range 21–52 years). No significant changes were observed for the active stand test or 6MWT. A significant reduction in insomnia severity (ISI: 16.6 vs. 13.6; p = 0.001) was observed post-intervention, but scores reverted toward baseline levels at 4-week follow-up. No significant improvements were seen in autonomic symptoms, anxiety, perceived stress, depression, well-being, or COVID-19 related distress. Pro-inflammatory CTRA gene expression decreased significantly from pre-to post-intervention (<em>p</em> = 0.004). Declines in CTRA gene expression were most significant among those with 3 COVID-19 positive events (<em>p</em> = 0.01), followed by 2 events (p = 0.04) and 1 event (p = 0.05). Declines in CTRA gene expression did not vary significantly as a function of recent illness, COVID-19 hospitalization, demographic characteristics, or general medical history.</div></div><div><h3>Conclusion</h3><div>A virtual, six-week mindfulness program may improve sleep quality in women with Long COVID dysautonomia. While no objective improvement in dysautonomia symptoms were observed, our findings suggest a favorable effect of the mindfulness intervention on inflammatory and antiviral biology with a decrease in CTRA gene expression. Nonetheless, the symptom burden in this population is very high, and more attention is needed to provide effective multi-modal clinical therapies to this population.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100963"},"PeriodicalIF":3.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune-neuroendocrine crosstalk in mood and psychotic disorders: A meta-analysis and systematic review","authors":"Minne Van Den Noortgate ,&nbsp;Filip Van Den Eede ,&nbsp;Violette Coppens ,&nbsp;Erik J. Giltay ,&nbsp;Livia De Picker ,&nbsp;Manuel Morrens","doi":"10.1016/j.bbih.2025.100965","DOIUrl":"10.1016/j.bbih.2025.100965","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Bidirectional interactions between immune and neuroendocrine mechanisms are involved in mood and psychotic disorders, although individual studies report inconsistent and even contradictory findings on the nature of this crosstalk. Our objective was to perform an up to date systematic review and meta-analysis of the association between hypothalamic-pituitary-adrenal (HPA) axis and immune system functioning in mood and psychotic disorders.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We searched the Pubmed, Web of Science and Embase databases for studies reporting correlations between one or more HPA- and immune markers (IM) in patients with mood or psychotic disorders. We analyzed unchallenged correlations as well as challenge studies investigating the HPA-immune interaction through dexamethasone (DEX) and/or CRH suppression, HPA-mediated challenge of immune cell proliferation, immune challenges, or psychological stressors. Finally, genetic studies focusing on HPA x immune interrelation were evaluated. For meta-analyzable data, three primary outcome measures were defined for immune functioning, namely the pro-inflammatory index (PII) and anti-inflammatory index (AII) for the molecular IM and a composite cellular immune marker score (CCIM) for the cellular IM. Secondary analyses were performed for the individual molecular and cellular IM. Heterogeneity was evaluated with the I&lt;sup&gt;2&lt;/sup&gt; statistic. Meta-regression analyses were performed to evaluate the impact of potential covariates (publication year, gender, age, symptom severity) on the primary outcome analyses.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;93 studies (n = 8226) were included, of which 50 (n = 5649) contained meta-analyzable data. The majority of the included studies (k = 72) investigated major depressive disorder (MDD) patients, nineteen schizophrenia spectrum disorders (SSD) and six bipolar disorder (BD). Under physiological conditions, a poor association was found between cortisol and the PII only in the unmedicated subsample of MDD (k = 8; n = 425; r = .205; z = 2.151; p = .031) and the medicated subsample of SSD (k = 4; n = 152; r = .0.237; z = 2.314; p = .021). No significant correlation was found in MDD between the AII and cortisol (k = 3; n = 1243; r = .005; z = .188; p = .851). Similar results were found for the association between immune cell numbers and cortisol in both MDD (k = 10; n = 773; r = −.005; z = −.113; p = .894) and SSD (k = 4; n = 99; r = .167; z = 1.356; p = .175). A total of 42 studies discussed post-challenge associations between immune alterations and HPA disturbances, of which 12 (n = 389; all MDD) contained meta-analyzable data and 37 entered the systematic review (n = 1783). No post-DEX correlations were found between cortisol and PII (k = 3; n = 105; r = .074; z = .355; p = .722) or CCIM (k = 5; n = 259; r = −.153; z = −1.294; p = .196). However, a significant association was found between post-DEX cortisol/ACTH and PII produced by sti","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100965"},"PeriodicalIF":3.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How does chronic psychosocial distress induce pain? Focus on neuroinflammation and neuroplasticity changes","authors":"Barbara Fülöp ,&nbsp;Éva Borbély ,&nbsp;Zsuzsanna Helyes","doi":"10.1016/j.bbih.2025.100964","DOIUrl":"10.1016/j.bbih.2025.100964","url":null,"abstract":"<div><div>Chronic primary pain including fibromyalgia for the musculoskeletal system persists for more than 3 months. Its etiological factors and the pathophysiological mechanisms are not known, and therefore, there is no satisfactory therapy, it is an unmet medical need condition. The only etiological and aggravating factor is chronic psychosocial distress, which is known to cause neuroimmune and endocrine changes both in the periphery and the central nervous system. In this short review, we introduce our research perspective by summarizing the recent literature on the interactions between chronic pain, stress, and commonly co-morbid mood disorders. Immune activation, autoimmunity, neuro-immune-vascular crosstalks and neuroinflammation play roles in the pathophysiology of these conditions. Data on stress-induced neuroplasticity changes at cellular and molecular levels were also collected in relation to chronic primary pain both from clinical studies and animal experiments of translational relevance. Understanding these mechanisms could help to identify novel therapeutic targets for chronic primary pain including fibromyalgia.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100964"},"PeriodicalIF":3.7,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143403025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding, predicting, and treating depression in pregnancy to improve mothers' and offspring's mental health outcomes: The HappyMums study","authors":"A. Biaggi ,&nbsp;V. Zonca ,&nbsp;C. Anacker ,&nbsp;V. Begni ,&nbsp;F. Benedetti ,&nbsp;A. Bramante ,&nbsp;A. Braniecka ,&nbsp;V. Brenna ,&nbsp;M. Bulgheroni ,&nbsp;C. Buss ,&nbsp;L. Cavaliere ,&nbsp;C.A.M. Cecil ,&nbsp;A.C. Couch ,&nbsp;D. de Barra ,&nbsp;H. El Marroun ,&nbsp;S. Entringer ,&nbsp;R. Grassi-Oliveira ,&nbsp;M. Jackowska ,&nbsp;A. Korosi ,&nbsp;P.J.C. Kwant ,&nbsp;A. Cattaneo","doi":"10.1016/j.bbih.2025.100961","DOIUrl":"10.1016/j.bbih.2025.100961","url":null,"abstract":"<div><h3>Background</h3><div>Perinatal depression is common: on average, more than 13% of women suffer from physician-diagnosed disorder and 20% report symptoms bearing clinical relevance. Maternal depression not only significantly impacts women's quality of life but also increases the offspring's risk of negative developmental outcomes, including mental disorders, through a combination of maternal alterations in <em>in-utero</em> biology and postnatal rearing factors during the early period of life. The HappyMums project aims to improve our understanding of perinatal depression by identifying the factors that robustly predict risk and resilience in mothers and their offspring, determining underlying neurobiological mechanisms, and, finally, testing the efficacy of potential interventions.</div></div><div><h3>Methods</h3><div>HappyMums will use data from a large collection of cohorts and registries containing biological, clinical, socio-demographic, environmental, and lifestyle data. It will pool unique human samples of maternal blood, placenta, chorionic villi and amniotic fluid, analyzing these data alongside pre-clinical samples of brain, blood and placental tissue from models of prenatal stress in mice and livebearing fish for correlative analyses. HappyMums will develop a mobile application (App) to collect multiple data types from women for early screening and monitoring of depressive symptoms.</div></div><div><h3>Conclusion</h3><div>The findings generated by HappyMums will be clinically relevant as they will increase the knowledge on perinatal depression, with unprecedented benefits for the offspring and the society as a whole.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100961"},"PeriodicalIF":3.7,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in the peripheral levels of cytokines during 12-month antipsychotic treatment in a drug-naïve schizophrenia spectrum cohort","authors":"I. Ratke ,&nbsp;A. Torsvik ,&nbsp;C.A. Bartz-Johannessen ,&nbsp;F. Fathian ,&nbsp;I. Joa ,&nbsp;S.M. Klæbo Reitan ,&nbsp;E.M. Løberg ,&nbsp;M. Rettenbacher ,&nbsp;S. Skrede ,&nbsp;V.M. Steen ,&nbsp;E. Johnsen ,&nbsp;R.A. Kroken","doi":"10.1016/j.bbih.2025.100959","DOIUrl":"10.1016/j.bbih.2025.100959","url":null,"abstract":"<div><h3>Background</h3><div>There are substantial sex differences in schizophrenia. However, research addressing sex differences regarding the antipsychotic effect on the immune system is lacking. The aim of our study was to compare changes in cytokine levels in men and women with schizophrenia spectrum disorder over 12 months of treatment with antipsychotics.</div></div><div><h3>Methods</h3><div>This study reports pre-planned secondary outcomes from the BeSt InTro Study – a pragmatic, semi-randomised, rater-blinded comparison of amisulpride, aripiprazole, and olanzapine. The groups were analysed collectively. Of the 144 enrolled patients with schizophrenia spectrum disorders and ongoing psychosis, 56 were antipsychotic-naïve at baseline (20 women and 36 men) and were included in this study. Blood samples from these 56 patients were drawn at baseline, prior to treatment with antipsychotics, and 1, 3, 6, 12, 26, 39, and 52 weeks after initiation of antipsychotic medication. Duration of treatment was 52 weeks. Serum cytokine levels were assessed with a multiplex immunoassay. Changes in the levels of IL-4, IL-6, TNF-α, IL-1β, IL-2, IL-10, IL-12p70, IL-17A, IFN-γ and CRP from baseline to the different follow-up times were analysed using linear mixed effects models separately for men and women, and then compared.</div></div><div><h3>Outcomes</h3><div>Cytokine levels were mainly stable in men during the study period. In women, IL-4 levels were lower at baseline compared with men (p = 0.048) and showed a consistent and significant increase at weeks 6 (p = 0.006), 26 (p &lt; 0.001), 39 (p = 0.002), and 52 (p = 0.001). TNF-α increased in women at weeks 26 (p = 0.008) and 39 (p = 0.012). IL-6 had a transient increase in women at weeks 12 (p = 0.003) and 26 (p = 0.007). There were significant sex differences in progression of cytokine levels at weeks 3 (IL-6: p = 0.046), 6 (IL-4: p = 0.022, IL-6: p = 0.015), 12 (IL-6: p = 0.01), 26 (IL-4: p &lt; 0.001, IL-6: p = 0.015, TNF-α: p = 0.026), 39 (IL-4: p = 0.003, TNF-α: p = 0.023) and 52 (IL-4: p &lt; 0.001, TNF-α: p = 0.009). CRP levels did not differ between sexes at baseline or during the study period and did not change significantly during treatment with antipsychotics in either sex.</div></div><div><h3>Interpretation</h3><div>We found significant sex differences in serum cytokine changes in drug-naïve patients with schizophrenia during treatment with antipsychotics. Cytokine levels were mainly altered in women, with increased IL-4, IL-6, and TNF-α levels. Cytokine changes may dramatically affect mental as well as somatic health. Our findings add to already established sex differences in schizophrenia pathophysiology and might have a potential role for future treatment guidelines.</div></div><div><h3>Funding</h3><div>The Research Council of Norway, the Western Norway Regional Health Trust, and the participating hospitals and universities provided funding for this study.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"44 ","pages":"Article 100959"},"PeriodicalIF":3.7,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143377215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early life psychosocial stress increases binge-like ethanol consumption and CSF1R inhibition prevents stress-induced alterations in microglia and brain macrophage population density","authors":"Stephen C. Gironda ,&nbsp;Samuel W. Centanni,&nbsp;Jeffrey L. Weiner","doi":"10.1016/j.bbih.2024.100933","DOIUrl":"10.1016/j.bbih.2024.100933","url":null,"abstract":"<div><div>Early life stress (ELS) has lasting consequences on microglia and brain macrophage function. During ELS, microglia and brain macrophages alter their engagement with synapses leading to changes in neuronal excitability. Further, ELS can induce innate immune memory formation in microglia and brain macrophages resulting in altered responsivity to future environmental stimuli. These alterations can result in lasting adaptations in circuit function and may mediate the relationship between ELS and the risk to develop alcohol use disorder (AUD). Whether microglia and brain macrophages truly mediate this relationship remains elusive. Here, we report: 1) an ELS model, psychosocial stress (PSS), increases binge-like ethanol consumption in early adulthood. 2) Repeated binge-like ethanol consumption increases microglia and brain macrophage population densities across the brain. 3) PSS may elicit innate immune memory formation in microglia and brain macrophages leading to altered population densities following repeated binge-like ethanol consumption. 4) Microglia and brain macrophage inhibition trended towards preventing PSS-evoked changes in binge-like ethanol consumption and normalized microglia and brain macrophage population densities. Therefore, our study suggests that acutely inhibiting microglia and brain macrophage function during periods of early life PSS may prevent innate immune memory formation and assist in reducing the risk to develop AUD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100933"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143082189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of high-sensitivity C-reactive protein with neuropsychological outcomes and cerebral white matter hyperintensities in older adults at risk of dementia","authors":"Rachael Yu ,&nbsp;Shawn D. Kong ,&nbsp;Catriona Ireland ,&nbsp;Genevieve Z. Steiner-Lim ,&nbsp;Kimberley Bassett ,&nbsp;Hannes Almgren ,&nbsp;Dongang Wang ,&nbsp;Chenyu Wang ,&nbsp;Johannes C. Michaelian ,&nbsp;Sharon L. Naismith","doi":"10.1016/j.bbih.2024.100924","DOIUrl":"10.1016/j.bbih.2024.100924","url":null,"abstract":"<div><div>Inflammation is becoming increasingly recognised as a core feature of dementia with evidence indicating that its role may vary and adapt across different stages of the neurodegenerative process. This study aimed to investigate whether the associations of high-sensitivity C-reactive protein (hs-CRP) with neuropsychological performance (verbal memory, executive function, processing speed) and cerebral white matter hyperintensities (WMHs) differed between older adults with subjective cognitive decline (SCD; <em>n</em> = 179) and mild cognitive impairment (MCI; <em>n</em> = 286). Fasting serum hs-CRP concentrations were grouped into low (&lt;1.0 mg/L), moderate (1.0–3.0 mg/L), and high (&gt;3.0–10.0 mg/L). Structural MRI scans were used to estimate WMH lesion volumes in the whole brain, as well as periventricular, deep white matter, and frontal regions. After adjusting for relevant demographic and clinical factors, multiple regression analyses revealed that in participants with SCD, high hs-CRP concentrations were significantly associated with poorer executive function (β[95% CI] = −.20[−.65, −.04], <em>p</em> = .025) and processing speed (β[95% CI] = −.19[−.53, .00], <em>p</em> = .048). Exploratory analyses suggested that this effect may be specific to APOE-ε4 non-carriers only. There were no significant associations between hs-CRP and neuropsychological outcomes in those with MCI. Hs-CRP was not associated with WMH volumes. Our findings suggest that hs-CRP may be involved in early disruptions to cerebral frontal-subcortical pathways, particularly in APOE-ε4 non-carriers, though this association may be independent of white matter lesions. In the earliest stages of cognitive decline where subjective complaints are paramount, addressing inflammation may offer potential benefits for supporting cognitive health.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100924"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11728901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142980941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinic evaluation of cognitive impairment in post-COVID syndrome: Performance on legacy pen-and-paper and new digital cognitive tests","authors":"Aysha Mohamed Rafik Patel ,&nbsp;Gina Gilpin ,&nbsp;Anna Koniotes ,&nbsp;Catherine Warren ,&nbsp;Cian Xu ,&nbsp;Paul W. Burgess ,&nbsp;Dennis Chan","doi":"10.1016/j.bbih.2024.100917","DOIUrl":"10.1016/j.bbih.2024.100917","url":null,"abstract":"<div><h3>Background</h3><div>Cognitive impairment, colloquially termed “brain fog”, is one of the most prevalent manifestations of post-Covid syndrome and a major contributor to impaired daily function and reduced quality of life. However, despite the high numbers of affected individuals presenting to clinical services with cognitive impairment, little work has been undertaken to date on the suitability of current memory clinic tests for identifying the cognitive deficits in this new acquired cognitive disorder.</div><div>The aim of this study was therefore to determine the performance of people with post-Covid syndrome presenting with cognitive impairment on the Addenbrooke's Cognitive Examination-III (ACE-III), a cognitive test used widely in memory clinics. A subset of individuals also underwent testing on a novel battery of short digital tests assessing attention, speed of information processing and executive function, representing the domains primarily implicated in post-Covid cognitive dysfunction.</div></div><div><h3>Methods</h3><div>102 individuals with post-Covid syndrome presenting with subjective cognitive complaints were recruited from a specialist cognitive long Covid clinic at University Hospitals Sussex NHS Trust. All participants completed self-report questionnaires on depression, anxiety, sleep and fatigue. Cognitive performance was assessed using the ACE-III, with 20 participants also being tested on the digital Long COVID Assessment Battery (LCCAB) (<em>N</em> = 20).</div></div><div><h3>Results</h3><div>The overall sample had a mean ACE-III score of 91/100 (SD 6) with 15.7% (16/102) scoring at or below the cut-off score considered to represent objective cognitive impairment. Of the 20 individuals who also completed the LCCAB, 89.47% were impaired on at least one task, primarily in the domains of attention, executive function and processing speed. Cognitive performance was not associated with depression, anxiety, sleep quality or fatigue.</div></div><div><h3>Conclusion</h3><div>The vast majority of individuals with post-Covid syndrome presenting with subjective cognitive complaints do not exhibit impaired performance on the ACE-III. This likely reflects the historical use of ACE-III and other pen and paper cognitive tests to detect cognitive impairment in diseases causing dementia, but they are ill-equipped to identify impairment in those cognitive domains affected in post-Covid syndrome. The LCCAB detected cognitive impairments in nearly 90% of participants, primarily affecting attention, executive function, and processing speed. These observations highlight the need for alternative cognitive tests for use in routine clinical practice to detect the impairments in new acquired cognitive disorders that are not adequately captured by legacy tests.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100917"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11665294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}