Brain, behavior, & immunity - health最新文献

{"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":"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":"Disease management teams in oncology: State of the art and the experience of a scientific institute of hospitalization and treatment (IRCCS) in Rome, Italy","authors":"Marialuisa Appetecchia ,&nbsp;Carlotta Amantea ,&nbsp;Marco Canfora ,&nbsp;Fabrizio Petrone ,&nbsp;Gennaro Ciliberto ,&nbsp;Ermete Gallo ,&nbsp;Laura Figorilli","doi":"10.1016/j.bbih.2024.100919","DOIUrl":"10.1016/j.bbih.2024.100919","url":null,"abstract":"<div><h3>Background</h3><div>This article analyzes the main coordination needs linked to the diagnosis and treatment of oncological diseases, presenting the various integration tools that our healthcare organization adopted to guarantee continuity of care at the IRCCS IFO (Istituto di Ricovero e Cura a Carattere Scientifico Istituti Fisioterapici Ospitalieri) in Rome. The object of investigation is the disease management team (DMT) organization for the diagnosis and treatment of people suffering from oncological disease and the consequences in terms of improving their management.</div></div><div><h3>Methods</h3><div>The study focuses, in particular, on the analysis of the different organizational methods chosen for the management of activities related to diagnosis and treatment paths.</div></div><div><h3>Results</h3><div>The results, although preliminary, highlight a great variability in the adoption of integrated organizational models by the different DMTs compatible with the heterogeneity of oncological diseases.</div></div><div><h3>Conclusion</h3><div>The results of this study have highlighted that, despite the diversity of the different DMTs created for different oncological pathologies, DMTs guarantee a patient-centered approach and the creation of shared databases, which facilitates the evaluation of progress and the identification of areas for improvement. This analysis has allowed us to obtain a useful map of the models used by the different DMTs, also laying the foundations for more precise evaluations of their effectiveness. The correct evaluation of the effectiveness of DMTs acquires great importance today, especially if we consider that empirical evidence is not yet in agreement on the real effectiveness of this tool with respect to both the qualitative dimension and the efficiency of interventions.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100919"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11713733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959759","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":"Trajectory of peripheral inflammation during index ECT in association with clinical outcomes in treatment-resistant depression","authors":"Christina M. Hough ,&nbsp;Jennifer L. Kruse ,&nbsp;Randall T. Espinoza ,&nbsp;John O. Brooks III ,&nbsp;Eliza J. Congdon ,&nbsp;Viviane Norris ,&nbsp;Michelle G. Craske ,&nbsp;Katherine L. Narr","doi":"10.1016/j.bbih.2024.100925","DOIUrl":"10.1016/j.bbih.2024.100925","url":null,"abstract":"<div><h3>Background</h3><div>Electroconvulsive therapy (ECT) is a highly efficacious intervention for severe and intractable depression. Evidence suggests ECT provokes an initial acute inflammatory response that subsequently decreases with repeated administration. However, relationships between inflammatory changes and clinical effects are unclear. Improved understanding of these processes may provide critical insight into effective intervention for treatment-resistant depression (TRD).</div></div><div><h3>Methods</h3><div>Plasma inflammatory markers were assessed at pre-treatment (T1), after the second ECT session (T2), and after ECT index series completion (post-treatment/T3) in TRD (n = 40). Changes were examined over time and in association with post-treatment Responder/Non-responder status (≥50% reduction in global depression severity) and percent change in affective, cognitive and neurovegetative depressive symptom domains.</div></div><div><h3>Results</h3><div>C-reactive protein (CRP) and interleukin-6 (IL-6) increased from pre-treatment to T2, and decreased from T2 to post-treatment. Neither early (%T2-T1) nor total (%T1-T3) change in inflammation predicted clinical outcomes, however, the interaction between early/acute inflammatory response and post-treatment inflammation (relative to baseline) was associated with clinical outcomes. Larger initial increases in IL-6 predicted greater reductions in both affective and cognitive symptoms in subjects with higher post-treatment IL-6; those with lower post-treatment IL-6 trended toward the opposite. The same was found between changes in CRP and neurovegetative symptoms.</div></div><div><h3>Conclusions</h3><div>Though preliminary, these results demonstrate how processes involved in the acute inflammatory response to ECT may differentially influence clinical outcomes depending on overall trajectory of inflammation following ECT. Findings also highlight the importance of examining symptom-specific changes in depression when studying treatment mechanisms, rather than relying solely on global measures of severity.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100925"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11743860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017379","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":"Measuring salivary cortisol in biobehavioral research: A systematic review and methodological considerations","authors":"Fanghong Dong ,&nbsp;Justine S. Sefcik ,&nbsp;Elizabeth Euiler ,&nbsp;Nancy A. Hodgson","doi":"10.1016/j.bbih.2024.100936","DOIUrl":"10.1016/j.bbih.2024.100936","url":null,"abstract":"<div><div>The assessment of salivary cortisol in community settings has gained popularity in biobehavioral research due to its noninvasive sampling, ease of handling and storage, and suitability for repeated sampling in short intervals. Ensuring consistent methodological practices for salivary cortisol is essential. This systematic review critically examines salivary cortisol collection procedures, data cleaning, and analysis to better understand its role in biobehavioral research within community populations. Fifty-eight articles met the inclusion criteria. Results indicated significant variability in study designs and cortisol measurement procedures, particularly regarding the biobehavioral role of cortisol, sampling periods, covariate considerations, cortisol analysis parameters, and data analysis plans. The review highlights commonly used and promising study designs while identifying methodological issues in cortisol measurement and analysis that should be addressed to improve comparability in future research.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100936"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048624","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}

{"title":"The association between hair cortisol and burnout is moderated by age, psychosocial, and immunological markers","authors":"Patrick D. Gajewski ,&nbsp;Peter Bröde ,&nbsp;Maren Claus ,&nbsp;Klaus Golka ,&nbsp;Jan G. Hengstler ,&nbsp;Carsten Watzl ,&nbsp;Edmund Wascher ,&nbsp;Stephan Getzmann","doi":"10.1016/j.bbih.2024.100909","DOIUrl":"10.1016/j.bbih.2024.100909","url":null,"abstract":"<div><h3>Background</h3><div>Exhaustion and depersonalization are the core symptoms of the occupational burnout. However, burnout is not an all-or-nothing phenomenon, but can occur in a milder to moderate form in otherwise healthy employees. In the last two decades hair cortisol concentrations (HCC) were increasingly related to the cumulative effect of psychosocial stress at work. We analyzed data of the Dortmund Vital Study (Clinicaltrials.gov: NCT05155397) to explore the relationship of HCC and burnout symptoms. Moreover, we asked whether the HCC – burnout association was moderated by work ability, chronic stress, neuroticism, depressive symptoms, and stress-related immunological biomarkers such as T cell concentration, CD4/CD8 cell ratio, and proinflammatory cytokines TNF- α, IL-6, and IL-18.</div></div><div><h3>Methods</h3><div>Burnout was assessed by the Oldenburg Burnout Inventory (OLBI), and the Maslach Burnout Inventory (MBI-D) in 196 working adults aged between 20 and 65 years (mean age 42.2 years). Several self-reported variables and biomarkers were collected.</div></div><div><h3>Results</h3><div>The results showed an association between HCC and the burnout measures. A series of moderator analyses revealed that the association between HCC and burnout symptoms was substantial for low work ability, high chronic stress level, high neuroticism level, and mild to moderate depressive symptoms. Immunological markers moderated the HCC – burnout association for high concentrations of T cells, low CD4/CD8 ratio and low IL-6, IL-18 and TNF-α concentrations. These interactions were moderated by age showing the largest impact in middle-aged to older individuals.</div></div><div><h3>Conclusions</h3><div>The present findings shed light on the complex interaction between burnout symptoms and work ability, chronic stress, personality, and the endocrinological and immunological responses across the working lifespan. These parameters should be considered when assessing the risk for developing burnout and validating the diagnosis of burnout.</div></div><div><h3>Trial registration</h3><div>ClinicalTrials.gov NCT05155397; <span><span>https://clinicaltrials.gov/ct2/show/NCT05155397</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100909"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883713","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":"Inflammatory proteins related to depression in multiple sclerosis: A systematic review and meta-analysis","authors":"L.A. Kiropoulos,&nbsp;V. Rozenblat,&nbsp;N. Baes","doi":"10.1016/j.bbih.2024.100939","DOIUrl":"10.1016/j.bbih.2024.100939","url":null,"abstract":"<div><h3>Background</h3><div>Up to 50% of individuals with multiple sclerosis (MS) experience depression. Depression has been accompanied by increases in inflammatory proteins. This meta-analysis summarized the data on inflammatory protein concentrations and level of depression in individuals with MS.</div></div><div><h3>Methods</h3><div>We performed a meta-analysis of studies measuring inflammatory protein concentrations and level of depression in individuals with MS with a database search of the English literature (to October 2024) and a manual search of references. Quality of evidence was also assessed.</div></div><div><h3>Results</h3><div>Fifteen studies involving measurements of inflammatory proteins and level of depression in 1102 individuals with MS were included in the meta-analysis: five for interleukin (IL)-10 (LPS and PHA), four for tumour necrosis factor (TNF)-α, four for interferon (IFN)-γ, and four for IL-6 (LPS and PHA). A meta-analysis showed that higher concentrations of TNF-α, IFN-γ, IL-6 and IL-10 were significantly associated with higher levels of depression in individuals with MS (<em>r</em> = 0.35, 95% CI [0.6,0.03], <em>p</em> = .015. Meta-analyses undertaken for individual inflammatory proteins of IFN-γ and IL-10 found positive associations between these proteins and level of depression although these did not reach statistical significance. Most studies were rated ‘poor quality’.</div></div><div><h3>Conclusion</h3><div>This meta-analysis reports significant associations between higher concentrations of TNF-α, IFN-γ, IL-6 and IL-10 and level of depresson in individuals with MS. Future longitudinal studies with improved reporting of data are needed to replicate these results and confirm the mechanisms through which these inflammatory proteins are present. Meta-analytic findings lend support to depression being associated with the activation of the inflammatory system in individuals with MS.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100939"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048865","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 role of CXCL12/CXCR4/CXCR7 axis in cognitive impairment associated with neurodegenerative diseases","authors":"Rojin Sarallah ,&nbsp;Shima Jahani ,&nbsp;Alireza Soltani Khaboushan ,&nbsp;Amir Kian Moaveni ,&nbsp;Maryam Amiri ,&nbsp;Masoumeh Majidi Zolbin","doi":"10.1016/j.bbih.2024.100932","DOIUrl":"10.1016/j.bbih.2024.100932","url":null,"abstract":"<div><div>Neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS), are characterized by progressive neuronal loss and cognitive impairment (CI). The: Cysteine-X-cysteine chemokine ligand 12(CXCL12)/CXC chemokine receptor type 4 (CXCR4)/CXC chemokine receptor type 7 (CXCR7) axis has emerged as a critical molecular pathway in the development of CI in these disorders. This review explores the role of this axis in the pathogenesis of CI across these neurodegenerative diseases, synthesizing current evidence and its implications for targeted therapies. In AD, dysregulation of this axis contributes to amyloid-β accumulation and tau hyperphosphorylation, leading to synaptic dysfunction and cognitive decline. PD studies reveal that CXCL12/CXCR4 signaling influences dopaminergic neuron survival and microglial activation, affecting cognitive function. In MS, the axis modulates neuroinflammation and demyelination processes, impacting cognitive performance. ALS research indicates that the CXCL12/CXCR4/CXCR7 pathway is involved in motor neuron degeneration and associated cognitive deficits. Across these diseases, the axis influences neuroinflammation, synaptic plasticity, and neuronal survival through various signaling cascades, including PI3K/AKT, MAPK, and JAK/STAT pathways. Emerging evidence suggests that modulating this axis could provide neuroprotective effects and potentially alleviate cognitive symptoms. This review highlights the potential of the CXCL12/CXCR4/CXCR7 axis as a therapeutic target for addressing CI in neurodegenerative diseases. It also underscores the need for further research to fully elucidate its role and develop effective interventions, potentially leading to improved clinical management strategies for these devastating disorders.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100932"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11743895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017376","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":"Inhibition of hippocampal interleukin-6 receptor-evoked signalling normalises long-term potentiation in dystrophin-deficient mdx mice","authors":"Kimberley A. Stephenson ,&nbsp;Aaron Barron ,&nbsp;Mark G. Rae ,&nbsp;Dervla O'Malley","doi":"10.1016/j.bbih.2024.100935","DOIUrl":"10.1016/j.bbih.2024.100935","url":null,"abstract":"<div><div>Duchenne muscular dystrophy (DMD), an X-linked neuromuscular disorder, characterised by progressive immobility, chronic inflammation and premature death, is caused by the loss of the mechano-transducing signalling molecule, dystrophin. In non-contracting cells, such as neurons, dystrophin is likely to have a functional role in synaptic plasticity, anchoring post-synaptic receptors. Dystrophin-expressing hippocampal neurons are key to cognitive functions such as emotions, learning and the consolidation of memories. In the context of disease-induced chronic inflammation, we have explored the role of the pleiotropic cytokine, interleukin (IL)-6 in hippocampal dysfunction using immunofluorescence, electrophysiology and metabolic measurements in dystrophic <em>mdx</em> mice. Hippocampal long-term potentiation (LTP) of the Schaffer collateral-CA1 projections was suppressed in <em>mdx</em> slices. Given the importance of mitochondria-generated ATP in synaptic plasticity, reduced maximal respiration in the CA1 region may impact upon this process. Consistent with a role for IL-6 in this observation, early LTP was suppressed in dystrophin-expressing wildtype slices exposed to IL-6. In dystrophic <em>mdx</em> mice, exposure to IL-6 suppressed mitochondrial-mediated basal metabolism in CA1, CA3 and DG hippocampal regions. Furthermore, blocking IL-6-mediated signalling by administering neutralising monoclonal IL-6 receptor antibodies intrathecally, normalised LTP in <em>mdx</em> mice. The impact of dystrophin loss from the hippocampus was associated with modified cellular bioenergetics, which underpin energy-driven processes such as the induction of LTP. The additional challenge of pathophysiological levels of IL-6 resulted in altered cellular bioenergetics, which may be key to cognitive deficits associated with the loss of dystrophin.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"43 ","pages":"Article 100935"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11762146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048274","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}