Brain, behavior, & immunity - health最新文献

{"title":"Changes of cognitive functions and proinflammatory cytokines across the lifespan in latent Toxoplasma gondii infection","authors":"Patrick D. Gajewski ,&nbsp;Peter Bröde ,&nbsp;Maren Claus ,&nbsp;Klaus Golka ,&nbsp;Jan G. Hengstler ,&nbsp;Jörg Reinders ,&nbsp;Carsten Watzl ,&nbsp;Edmund Wascher ,&nbsp;Stephan Getzmann","doi":"10.1016/j.bbih.2025.101105","DOIUrl":"10.1016/j.bbih.2025.101105","url":null,"abstract":"<div><h3>Background</h3><div>Recent findings showed serious consequences of latent <em>T. gondii</em> infection on the central nervous system, leading to psychiatric, immunological and cognitive impairments. However, little is known about the temporal dynamics of the latent <em>T. gondii</em> infection in respect to immunological and cognitive changes across the adult life span. The present study aims at evaluating the course of cognitive changes across the adult life span in relation to latent <em>T. gondii</em> infection and the interplay with proinflammatory cytokines leading to chronic inflammation as a potential origin of the cognitive decline in infected adults.</div></div><div><h3>Methods</h3><div>In a double-blinded cross-sectional design, data of 218 seropositive and 475 seronegative adults aged between 20 and 88 years were compared regarding crucial cognitive domains: processing speed, working memory, immediate and delayed memory, sustained attention, and executive functions. In a subsample of up to 300 participants, concentrations of proinflammatory cytokines IL-6, IL-8, IL-18, and TNF-α were analyzed to evaluate their interaction with <em>T. gondii,</em> and to determine whether the cytokines interact in their effects on cognition across the lifespan.</div></div><div><h3>Results</h3><div>The results showed an interaction between age and <em>T. gondii</em> status, with a decline in cognitive performance in infected, relative to non-infected, older individuals, and the reversed pattern in young to middle-aged adults. Specifically, this pattern was evident in working memory, immediate and delayed recall, as well as switching ability. Age was associated with increased levels of proinflammatory cytokines, and reduced concentration of <em>T. gondii</em> antibodies. IL-6, IL-8 and TNF-α levels were negatively associated with <em>T. gondii</em> antibody level and cognitive performance. Finally, <em>T. gondii</em> interacted with IL-6, IL-8 and TNF-α, predicting superior performance in immediate and delayed memory tasks in younger adults with high levels of <em>T. gondii</em> IgG antibodies and cytokines, whereas <em>T. gondii</em> IgG antibody and cytokine levels played less of a role for these functions in older age.</div></div><div><h3>Conclusion</h3><div>The findings support a model of dynamically shifting effects of <em>T. gondii</em> and proinflammatory cytokines on the central nervous system and cognition with increasing age, suggesting positive effects of <em>T. gondii</em> infections in younger adults, and neuroinflammatory effects in older age presumably due to chronic inflammation. Given the high prevalence of latent toxoplasmosis in the general population and the growing population of older adults, these findings are of relevance for public health.</div></div><div><h3>Trial registration</h3><div>Clinicaltrials.gov NCT05155397.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101105"},"PeriodicalIF":3.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145097899","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}

{"title":"Exploratory study of the dysregulation of age-related changes in neural/glial antigen 2 and neuroinflammation markers in individuals with major depression","authors":"Javier Vargas-Medrano,&nbsp;Diana Sotelo,&nbsp;Guadalupe Vidal Martínez,&nbsp;Peter M. Thompson","doi":"10.1016/j.bbih.2025.101107","DOIUrl":"10.1016/j.bbih.2025.101107","url":null,"abstract":"<div><div>Aging involves the alteration of the central nervous system myelin, which is produced by oligodendrocytes. These cells originate from oligodendrocyte precursor [neural/glial antigen 2 (NG2)] cells, which are influenced by neuroinflammatory processes. Neuroinflammatory activity contributes to accelerated aging in individuals with mental illnesses such as major depressive disorder (MDD). This study was conducted to better understand the anti- and pro-neuroinflammatory changes associated with NG2 cells in aging individuals with MDD. Human postmortem dorsolateral prefrontal cortex samples were obtained from adults with MDD and normal controls (NCs) of different ages. Western blotting was performed to measure the protein levels of the oligodendrocyte progenitor cell marker NG2, the inflammatory markers interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α), hepatocyte growth factor (HGF), and the anti-inflammatory neuronal viability marker B-cell lymphoma 2 (Bcl-2). Age-related changes in these markers were examined by simple linear regression. In NCs, the levels of NG2 and HGF increased linearly with age (<em>p</em> = 0.04 and <em>p</em> = 0.02, respectively), and the Bcl-2 level tended to follow the same trend (<em>p</em> = 0.08). The IL-1β and TNF-α levels were not significantly associated with age in NCs (<em>p</em> = 0.96 and <em>p</em> = 0.67, respectively). In the MDD group, a linear relationship with age was observed for the HGF level (<em>p</em> = 0.03) but not the NG2 (<em>p</em> = 0.23) or Bcl-2 (<em>p</em> = 0.92) level. Trends toward significant positive linear relationships with age were observed for the levels of IL-1β (<em>p</em> = 0.06) and TNF-α (<em>p</em> = 0.08). Our data suggest that brain aging is advanced in individuals with MDD in part due to increased neuroinflammation and reduced pro-survival protein levels and myelination potential.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101107"},"PeriodicalIF":3.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145097898","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}

{"title":"Heritability of neonatal acute phase protein levels","authors":"Hugo Sjöqvist ,&nbsp;Martin Brynge ,&nbsp;Kristiina Tammimies ,&nbsp;Ralf Kuja-Halkola ,&nbsp;Sven Bölte ,&nbsp;Christina Dalman ,&nbsp;Renee M. Gardner ,&nbsp;Håkan Karlsson","doi":"10.1016/j.bbih.2025.101097","DOIUrl":"10.1016/j.bbih.2025.101097","url":null,"abstract":"<div><div>Levels of neonatal Acute Phase Proteins (APPs) have been associated with autism and schizophrenia. The relative contributions of genetic and environmental factors to variation in APP levels in the neonatal period are not known. Therefore, we used one of the largest twin samples to date to map the proportions of heritable and non-heritable factors to variations in APPs measured shortly after birth. Moreover, we investigated if any association existed between neonatal APP levels and autism, among monozygotic and dizygotic twins discordant for autism.</div><div>Twins were identified and enrolled from registers and a clinical twin study of autism in Sweden. The distributions of APPs measured in dried blood spots taken a few days after birth as part of a national screening program were standardized to reduce any analytical artifacts. The additive genetic (A), common (C) and unique (E) environment components were estimated, using the ACE model, on a sample of 92 twin pairs. We included 61 autism discordant twin pairs for estimating the association between the APPs and autism, using both non-fixed (between) and fixed (within) effects regression models.</div><div>For the ACE models, variations in α-2 macroglobulin, C-reactive protein, ferritin, fibrinogen, haptoglobin, serum amyloid A and serum amyloid P were all largely explained by additive genetic factors (70–90 %). Variation in tissue plasminogen activator and procalcitonin were predominantly explained by common environmental factors (60–70 %) with a negligible contribution by genetic factors. Variations in levels of tissue plasminogen activator and procalcitonin in the neonatal period appear to be mainly explained by pregnancy and birth related factors. Variations in levels of other investigated acute phase proteins were largely explained by additive genetic factors. None of the APPs exhibited any significant association with autism in discordant mono- or dizygotic twin pairs. Our findings highlight the importance of considering potential familial confounding in future studies of association between any APP and autism.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101097"},"PeriodicalIF":3.5,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145061576","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}

{"title":"Associations of lifetime stressors and health behaviors with inflammation in young adults previously placed in youth residential care","authors":"David Bürgin ,&nbsp;Kristen Nishimi ,&nbsp;Vera Clemens ,&nbsp;Maria Meier ,&nbsp;Eva Unternaehrer ,&nbsp;Laura Gurri ,&nbsp;Evelyne Bruttin ,&nbsp;Nicolas Rohleder ,&nbsp;Paul Klauser ,&nbsp;Daniella Dwir ,&nbsp;Nimmy Varghese ,&nbsp;Anne Eckert ,&nbsp;Süheyla Seker ,&nbsp;Delfine d’Huart ,&nbsp;Cyril Boonmann ,&nbsp;Marc Schmid ,&nbsp;Aoife O'Donovan","doi":"10.1016/j.bbih.2025.101098","DOIUrl":"10.1016/j.bbih.2025.101098","url":null,"abstract":"<div><h3>Background</h3><div>Early life stressors (ELS) and stressful life events (SLEs) increase the risk for various physical health conditions, and health behaviors can modulate stress-associated risks. A key mechanism linking both lifetime stress and health behaviors with physical health outcomes is chronic low-grade inflammation. However, it is unclear how both stressor exposure and more proximal health behaviors are associated with inflammation in highly stress-exposed groups.</div></div><div><h3>Objectives</h3><div>Here, we investigated associations of lifetime stressors and health behaviors with peripheral inflammation in a highly stress exposed sample of young adults previously placed within youth residential care in Switzerland.</div></div><div><h3>Method</h3><div>We examined 126 young adults (<em>M</em>_Age = 26.3 years; 31 % female) who completed questionnaires to assess ELS, SLEs, and risky and protective health behaviors. Inflammatory markers (C-reactive protein [CRP], interleukin [IL]-6, tumor necrosis factor [TNF]-α, IL-10, and IL-1ra) were measured in venous blood using high sensitivity enzyme-linked immunosorbent assays (hsELISAs). Regressions estimated associations between ELS, SLEs, and health behaviors with each inflammatory marker.</div></div><div><h3>Results</h3><div>Our sample reported high levels of ELS and SLEs, as well as high levels of risky health behaviors. ELS and SLEs were mostly unassociated with young adult health behaviors, and both ELS and SLEs were not associated with inflammatory markers, adjusting for covariates. Regarding behavior, nicotine dependence was associated with higher pro-inflammatory markers and alcohol abuse marginally with a lower anti-inflammatory marker, while physical activity and better sleep quality were associated with lower pro-inflammatory markers, adjusting for covariates.</div></div><div><h3>Conclusions</h3><div>Among individuals with high levels of lifetime stress, cumulative ELS and SLEs were unassociated with inflammation, whereas risky behaviors were associated with higher, and protective behaviors with lower inflammatory markers. Interventions that reduce risky and promote protective health behaviors may lower inflammation and promote long-term health among individuals who have experienced high lifetime stressors exposure.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101098"},"PeriodicalIF":3.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145057403","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}

{"title":"Induction of endogenous IL-10 promotes resolution and tolerance of nitric oxide in microglia","authors":"Hsing-Chun Kuo ,&nbsp;Jia-Shing Chen ,&nbsp;Chun-Nun Chao ,&nbsp;Kam-Fai Lee ,&nbsp;Yi-Te Huang ,&nbsp;Pin-Cheng Mao ,&nbsp;Tzu-Chia Lin ,&nbsp;Shu-Chen Chiu ,&nbsp;Ya-Ling Huang ,&nbsp;Chun-Hsien Chu","doi":"10.1016/j.bbih.2025.101094","DOIUrl":"10.1016/j.bbih.2025.101094","url":null,"abstract":"<div><div>Endogenous interleukin-10 (IL-10), a potent anti-inflammatory cytokine, is induced in a timely and coordinated manner to dampen microglia-mediated brain inflammation. However, it remains unclear how it alters the inflammatory process to shape the immune polarization of microglia. This study aimed to investigate the anti-inflammatory mechanisms of endogenous IL-10 in activated and tolerized microglia using in vitro multiple-reconstituted primary brain cell cultures and an in vivo IL-10 knockout (IL-10KO) animal model. Upon a single or repeated lipopolysaccharide (LPS) treatment regimen, the expression levels of the inflammatory factors during the neuroinflammatory/tolerance process were measured by quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA), and Griess reagent assay. ELISA data showed that cell-autonomous induction of endogenous IL-10 occurs in LPS-activated and LPS-tolerized microglia. Furthermore, comparing the LPS-elicited pro-inflammatory factor expressions at different neuroinflammatory stages between the wild-type and IL-10KO groups, our data revealed the failure of negative-feedback suppression of inducible nitric oxide synthesis (iNOS) during immune resolution in the IL-10KO brains. Moreover, LPS-treated IL-10KO microglia increase the supernatant level of nitrite and become overactive during late-stage inflammation, despite no changes in cell number; in contrast, LPS-tolerized IL-10KO microglia fail to program endotoxin tolerance of nitric oxide/inducible nitric oxide synthesis (iNOS). In summary, our data demonstrate that the cell-autonomous induction of endogenous IL-10 in microglia is crucial for mitigating brain immune responses, particularly in the resolution and tolerance of nitric oxide.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"49 ","pages":"Article 101094"},"PeriodicalIF":3.5,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145050593","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}

{"title":"Cumulative social advantage is associated with slower epigenetic aging and lower systemic inflammation","authors":"Anthony D. Ong ,&nbsp;Frank D. Mann ,&nbsp;Laura D. Kubzansky","doi":"10.1016/j.bbih.2025.101096","DOIUrl":"10.1016/j.bbih.2025.101096","url":null,"abstract":"<div><h3>Background</h3><div>Social relationships are established determinants of health across the lifespan, yet the cumulative and multidimensional effects of sustained social advantage on biological aging remain poorly understood.</div></div><div><h3>Methods</h3><div>Drawing on data from 2117 adults in the Midlife in the United States (MIDUS) study, we used structural equation modeling to examine whether cumulative social advantage (CSA)—a latent construct encompassing social connection across familial, religious, emotional, and community domains—was associated with epigenetic aging, systemic inflammation, and neuroendocrine activity.</div></div><div><h3>Results</h3><div>Higher CSA was linked to slower epigenetic aging, particularly as indexed by GrimAge (β = −0.09 to −0.10, <em>q</em> &lt; 0.001) and DunedinPACE (β = −0.12, <em>q</em> = 0.010) clocks. CSA was also associated with lower levels of interleukin-6 (IL-6; β = −0.11, <em>q</em> = 0.010). No significant associations were observed for urinary cortisol, cortisone, or catecholamines.</div></div><div><h3>Conclusion</h3><div>Sustained social advantage is associated with more favorable biological aging profiles, including slower epigenetic aging and reduced inflammatory signaling. These findings add to growing evidence that social resources are embedded in the physiological pathways that shape aging and health.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101096"},"PeriodicalIF":3.5,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145018482","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}

{"title":"The predictivity of hematological parameters and related inflammatory biomarkers of male subjects with chronic polysubstance use disorder","authors":"Mohammad A. Bani-Ahmad ,&nbsp;Belal A. Al-Husein ,&nbsp;Diala Q. Alshaabi ,&nbsp;Duaa A. Aldmour ,&nbsp;Yasmeen E. Ghanim ,&nbsp;Rahaf F. Al Deqah","doi":"10.1016/j.bbih.2025.101095","DOIUrl":"10.1016/j.bbih.2025.101095","url":null,"abstract":"<div><h3>Background</h3><div>Polysubstance use disorder (PSUD) is a chronic disease with adverse clinical outcomes. Hematological properties and related inflammatory biomarkers have not been investigated in PSUD. This study aimed to investigate the alterations in hematologic and related inflammatory parameters among subjects with PSUD.</div></div><div><h3>Methods</h3><div>A total of sixty subjects were included, thirty chronic PSUD subjects and thirty control subjects. Venous blood was withdrawn from participants, and complete blood count was conducted. Related inflammatory biomarkers were calculated, including neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), neutrophil-to-monocyte ratio (NMR), derived neutrophil-to-lymphocyte ratio (dNLR), and systemic inflammation index (SII).</div></div><div><h3>Results</h3><div>Between study groups, we reported significant differences in red cell count, hematocrit, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration (P &lt; 0.001). As compared to control subjects, PSUD subjects had significantly higher neutrophil counts that coincided with significantly lower monocyte counts (P &lt; 0.001). These findings corresponded to significantly higher NLR (2.88 ± 0.21 vs. 1.92 ± 0.13), dNLR (2.39 ± 0.97 vs.1.43 ± 0.08), NMR (35.1 ± 4.8 vs.8.3 ± 0.5), LMR (13.3 ± 1.7 vs. 4.6 ± 0.3) and SII (683.0 ± 56.9 vs. 424.3 ± 30.2) among PSUD subjects (P &lt; 0.001). Receiver operating characteristic analysis revealed areas under the curves for NMR, LMR, dNLR, NLR, and SII of 0.983, 0.829, 0.811, 0.766, and 0.779, respectively (P &lt; 0.001).</div></div><div><h3>Conclusion</h3><div>Chronic PSUD alters erythrocyte indices that define mild erythrocytic hyperchromasia and may suggest membrane damage. Furthermore, higher hematological inflammatory biomarkers imply the contribution of systemic inflammation in the pathophysiology of PSUD and suggest their diagnostic predictivity of the disease.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101095"},"PeriodicalIF":3.5,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913120","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}

{"title":"Neurocognitive trajectories in long COVID: Evidence from longitudinal analyses","authors":"Jacqueline H. Becker ,&nbsp;Jia Li ,&nbsp;Jenny J. Lin ,&nbsp;Alex Federman ,&nbsp;Emilia Bagiella ,&nbsp;Minal S. Kale ,&nbsp;Daniel Fierer ,&nbsp;Logan Bartram ,&nbsp;Juan P. Wisnivesky","doi":"10.1016/j.bbih.2025.101093","DOIUrl":"10.1016/j.bbih.2025.101093","url":null,"abstract":"<div><h3>Background</h3><div>Patients frequently report symptoms of cognitive impairment or “brain fog” after acute COVID-19 infection, but the trajectory of these symptoms over time has yet to be determined. We assessed cognitive function over a 42-month period after acute SARS-CoV-2 infection and identified factors associated with the trajectory of cognitive function over this period.</div></div><div><h3>Methods</h3><div>We analyzed data from participants in the Mount Sinai Health System Post-COVID-19 Registry in New York City, a prospective cohort study of adults followed after acute SARS-CoV-2 infection of any severity. Participants were identified from a list of all patients with COVID-19 who received care at an MSHS facility in New York, recruited beginning April 2020 and followed through January 2024. Cognition was assessed using well-validated in-person measures of attention, working memory, processing speed, executive functioning, language, and memory. We used linear mixed models to investigate the relationships between cognitive scores and time. We also assessed factors (including race, ethnicity, site of acute COVID-19 care, fatigue, depression, anxiety, body mass index, medical comorbidities, and COVID-19 vaccination) that may influence changes in cognitive scores over time.</div></div><div><h3>Findings</h3><div>We analyzed data from 1553 participants (median age 53 years, 63 % female, 17 % Black, 21 % Hispanic). In adjusted analyses, scores from cognitive measures of attention, working memory, processing speed, executive functions, and verbal learning and memory improved progressively through 42 months post-COVID. However, despite the improvements, on average, measures of processing speed and executive functioning remained ≥1 standard deviation below the normative mean. Having a body mass index of &lt;25 kg/m² was predictive of a greater improvement in cognitive scores.</div></div><div><h3>Interpretation</h3><div>While cognitive impairment occurring after COVID-19 improved over time in most domains, processing speed and executive functioning remained below the normal range. The cognitive health burden of Long COVID is therefore significant and lasting. Future studies should examine interventions to support rapid recovery, as well as dynamic risk prediction models to determine factors that may impact cognitive recovery longer term.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101093"},"PeriodicalIF":3.5,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144916677","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}

{"title":"Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder","authors":"Albert Frank Magnusen ,&nbsp;Robert James Hopkin ,&nbsp;Charles Vorhees ,&nbsp;Elizabeth Wilson ,&nbsp;Molly Moehlman ,&nbsp;Barbara Hallinan ,&nbsp;Craig Erickson ,&nbsp;Melissa P. DelBello ,&nbsp;Luca Marsili ,&nbsp;Nicole G. Coufal ,&nbsp;Manoj Kumar Pandey","doi":"10.1016/j.bbih.2025.101091","DOIUrl":"10.1016/j.bbih.2025.101091","url":null,"abstract":"<div><div>Adenylosuccinate lyase deficiency disorder (ADSLDD) is an ultra-rare autosomal recessive metabolic condition that leads to severe neurological impairment, with an estimated global prevalence of approximately 0.00125 cases per 100,000 individuals. Clinically, ADSLDD presents in three distinct phenotypes: the fatal neonatal form, the childhood form, and the more slowly progressive form, each characterized by varying degrees of developmental and neurological dysfunction. The disorder is caused by pathogenic variants in the ADSL gene, leading to impaired enzymatic activity and the accumulation of toxic substrates particularly succinyladenosine (S-Ado) and succinylaminoimidazole carboxamide riboside (SAICAr).</div><div>The ratio of S-Ado to SAICAr in cerebrospinal fluid has been correlated with disease severity, where lower ratios are associated with more severe clinical outcomes. However, the precise mechanisms linking elevated SAICAr levels to neurological damage remain incompletely understood.</div><div>This review summarizes current insights into the metabolic dysfunction and immune activation observed in ADSLDD, with a focus on the role of SAICAr in promoting neuroinflammation. We highlight emerging hypotheses implicating activation of the alternative complement pathway as a key driver of inflammation, blood-brain barrier disruption, and progressive neurodegeneration.</div><div>By synthesizing recent findings, this review underscores the urgent need for mechanistic studies and therapeutic exploration, particularly targeting complement activation, as a promising strategy to mitigate inflammation and improve clinical outcomes in ADSLDD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101091"},"PeriodicalIF":3.5,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144890094","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}

{"title":"The role of music in perinatal mental health, with a psychoneuroimmunological perspective","authors":"Kiran Kuri,&nbsp;Rebecca H. Bind,&nbsp;Lavinia Rebecchini","doi":"10.1016/j.bbih.2025.101092","DOIUrl":"10.1016/j.bbih.2025.101092","url":null,"abstract":"<div><div>Music has a profound and widespread impact, fostering social connectedness across diverse cultural, ethnic, and socioeconomic groups. It plays a significant role in individuals’ lives – used for relaxation, emotional expression, and entertainment. In recent years, a growing body of research has demonstrated the therapeutic potential of music in both mental and physical health contexts. Music-based interventions have been successfully employed in a range of clinical settings, including for the management of anxiety, depression, and autism spectrum disorder. Emerging evidence has highlighted the role of music in supporting perinatal mental health. Studies indicate that music-based interventions can ease anxiety and depressive symptoms during pregnancy and the postnatal period, promote maternal-infant bonding, and assist women in coping during labour. These interventions are increasingly used due to their cost-effectiveness, accessibility, and suitability for individuals with limited verbal communication abilities. Researchers have also begun to explore the psychoneuroimmunological mechanisms that may underlie these effects. This article aims to explore and synthesise current evidence on how music can support perinatal mental health, while examining the biological and psychological pathways through which these benefits may arise.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101092"},"PeriodicalIF":3.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879149","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}