Brain, behavior, & immunity - health最新文献

{"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}

{"title":"Psychological distress in older adults: associations with epigenetic markers of ageing, inflammation, and depression, and joint effects on mortality","authors":"Danmeng Lily Li ,&nbsp;Xiaojing Xu ,&nbsp;Allison M. Hodge ,&nbsp;Melissa C. Southey ,&nbsp;Graham G. Giles ,&nbsp;Roger L. Milne ,&nbsp;Pierre-Antoine Dugué","doi":"10.1016/j.bbih.2025.101090","DOIUrl":"10.1016/j.bbih.2025.101090","url":null,"abstract":"<div><h3>Background</h3><div>Psychological distress is associated with adverse health outcomes. We aimed to assess whether the health impacts of psychological distress could be captured by epigenetic markers of ageing, inflammation, and depression, and whether these markers and psychological distress have a synergistic association with mortality in older Australians.</div></div><div><h3>Methods</h3><div>Blood DNA methylation data for 1146 participants (31 % females, mean age: 69 years) in the Melbourne Collaborative Cohort Study were used to calculate epigenetic markers of ageing (<em>PCPhenoAge</em>, <em>PCGrimAge</em>, <em>bAge</em>, <em>DunedinPACE</em>) and inflammation (C-reactive protein [<em>mCRP</em>]), and two methylation scores for depression. Psychological distress was assessed by the Kessler scale (K10). Linear regression was used to assess the associations of K10 with epigenetic markers. Cox models were used to assess the multiplicative and additive interactions of K10 and epigenetic markers in their association with all-cause mortality.</div></div><div><h3>Results</h3><div>We observed positive associations of K10 with epigenetic markers of ageing and inflammation: per standard deviation (SD), 0.05 (95 %CI: 0.00–0.11) for <em>DunedinPACE</em> to 0.10 (95 %CI: 0.05–0.16) for <em>PCPhenoAge</em>. Associations of epigenetic markers of ageing with mortality were stronger in participants with higher psychological distress. The relative excess risk due to interaction for <em>DunedinPACE</em> was 0.82, 95 %CI: 0.14–1.50.</div></div><div><h3>Conclusion</h3><div>In older Australians, higher psychological distress was associated with older epigenetic age and higher <em>mCRP</em>. Participants with higher levels of both psychological distress and epigenetic markers of ageing and <em>mCRP</em> had higher mortality risk. These findings highlight links between psychological and biological health, and the potential importance of considering both for disease risk stratification.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101090"},"PeriodicalIF":3.5,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879148","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":"Biomarker-based profiling of fatigue in childhood cancer survivors: evidence for distinct inflammatory and glial-associated profiles","authors":"Deveny Vanrusselt ,&nbsp;Sabine Verschueren ,&nbsp;Lize Van Meerbeeck ,&nbsp;Jurgen Lemiere ,&nbsp;Stephanie Humblet-Baron ,&nbsp;Charlotte Sleurs ,&nbsp;Anne Uyttebroeck","doi":"10.1016/j.bbih.2025.101089","DOIUrl":"10.1016/j.bbih.2025.101089","url":null,"abstract":"<div><h3>Background</h3><div>Fatigue is a prevalent and burdensome late effect in childhood cancer survivors (CCS), yet its biological underpinnings remain poorly understood. This study examined associations between fatigue and blood-based biomarkers in CCS compared to healthy controls (HCs) and explored whether biologically distinct CCS profiles with respect to fatigue could be identified.</div></div><div><h3>Procedure</h3><div>Eighty CCS (aged 14–28) and 35 age- and sex-matched HCs provided blood samples and completed the Pediatric Quality of Life Inventory Multidimensional Fatigue Scale (PedsQL-MFS). Plasma concentrations of 12 biomarkers (e.g., IL-2, TNF-α, BDNF, Total Tau, NfL, MCP-1, GFAP) were quantified using Meso Scale Discovery immunoassays. Analyses included group comparisons, Spearman correlations, and unsupervised clustering (hierarchical and k-means).</div></div><div><h3>Results</h3><div>CCS reported significantly higher fatigue than HCs and showed significantly elevated levels of GFAP (d = 0.43), MCP-1 (d = 0.74), and Total Tau (d = 0.54). No individual biomarkers differentiated fatigued from non-fatigued CCS. Clustering revealed two biomarker-based CCS subgroups: one with high levels of inflammatory and neurodegenerative markers, and one with lower levels, yet fatigue severity was comparable. Within-cluster analyses showed distinct patterns: in the low-biomarker group, fatigue was associated with GFAP (ρ = −0.26 and ρ = −0.27, p &lt; 0.05), whereas in the high-biomarker group, fatigue was more consistently linked to IL-8, IL-1α, and TNF-α (ρ = −0.38 to −0.49, p &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Findings suggest that fatigue in CCS may be associated with distinct biological pathways, including astrocyte-linked processes in one subgroup and systemic inflammation in another. This suggests the need for more personalized, biomarker-informed strategies to understand and manage fatigue in pediatric cancer survivorship.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101089"},"PeriodicalIF":3.5,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826918","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":"Acute systemic endotoxin administration elevates neuroimmune markers and sickness behaviors in male and female Peromyscus californicus","authors":"Amy J. Wegener ,&nbsp;Hannah Stadtler ,&nbsp;Hannah D. Fulenwider ,&nbsp;Erica R. Glasper ,&nbsp;Gretchen N. Neigh","doi":"10.1016/j.bbih.2025.101087","DOIUrl":"10.1016/j.bbih.2025.101087","url":null,"abstract":"<div><div>The California mouse is a biparental monogamous rodent species used to study the neuroendocrine mechanisms underlying social stressors, but there is limited research investigating the neuroimmune response within the species to facilitate our understanding of stress and neuroinflammation interactions. The data herein provide an assessment of behavior, somatic metrics, and gene expression changes within the prefrontal cortex (PFC) and hippocampus (HPC) at 4- and 24-h following a single peripheral injection of the endotoxin lipopolysaccharide (LPS) in males and females. We observed effects of LPS on spleen weights and both males and females demonstrated sickness-like behaviors at 24 h as indicated by assessment of nest building quality. Within both sexes in both the PFC and HPC, proinflammatory genes (i.e., tumor necrosis factor (TNF) and interleukin-1β (IL-1β)) were increased at 4 h following LPS, with a return towards expression levels of saline controls by 24 h. Gene expression of GFAP, Cd68, and Complement C3 were elevated by LPS in both sexes and both brain regions with highest expression observed at 24 h. Given that mitochondria function is impacted by inflammatory mediators, we isolated functional synaptic mitochondria to assess for changes in oxygen consumption. Mitochondria spare capacity was elevated in the PFC 4 h after LPS, but only in males. LPS did not alter mitochondrial function at any time point within the HPC for either sex. Collectively, these data demonstrate that both male and female California mice exhibit peripheral and neuroinflammatory consequences of an acute LPS challenge with relative sparing of synaptic mitochondrial function. These data provide a framework for building California mouse studies focused on the intersection of social stress and inflammation on behavioral outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101087"},"PeriodicalIF":3.5,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842832","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":"Anxiety and nonpsychotic mental disorders in acute urticaria","authors":"Eli Magen ,&nbsp;Eugene Merzon ,&nbsp;Shai Ashkenazi ,&nbsp;Abraham Weizman ,&nbsp;Iris Manor ,&nbsp;Israel Magen ,&nbsp;Avi Yakov ,&nbsp;Akim Geishin ,&nbsp;Ilan Green ,&nbsp;Avivit Golan-Cohen ,&nbsp;Shlomo Vinker ,&nbsp;Ariel Israel","doi":"10.1016/j.bbih.2025.101088","DOIUrl":"10.1016/j.bbih.2025.101088","url":null,"abstract":"<div><h3>Background</h3><div>Acute urticaria (AU) is characterized by the sudden onset of wheals, angioedema, or both, with symptoms resolving within 6 weeks. While the association between chronic urticaria and mental health disorders is well-documented, the relationship between AU and psychological conditions remains understudied.</div></div><div><h3>Objective</h3><div>To investigate the association between AU and anxiety and personality disorders, and to explore the potential psychoneuroimmunological mechanisms underlying these relationships.</div></div><div><h3>Methods</h3><div>We conducted a population-based case-control study using the comprehensive electronic health records database of Leumit Health Services in Israel. The study included 72,805 AU patients and 291,220 matched controls. Subjects were matched for gender, age, ethnicity, year of first documented visit, and socioeconomic status. We analyzed the 20-year prevalence of anxiety disorders, personality disorders, and various nonpsychotic mental disorders in both groups.</div></div><div><h3>Results</h3><div>AU patients demonstrated significantly higher prevalence of anxiety disorders (7.02 % vs. 5.22 %, <em>p &lt; 0.001</em>, OR = 1.37 [95 % CI: 1.33–1.42]), personality disorders (0.23 % vs. 0.134 %, <em>p &lt; 0.001</em>, OR = 1.73 [95 % CI: 1.44–2.08]), and adjustment disorders (0.91 % vs. 0.67 %, <em>p &lt; 0.001</em>, OR = 1.37 [95 % CI: 1.25–1.50]) compared to controls. Particularly notable were the associations with personality disorders characterized by persistent mood disturbances (OR = 1.91 [95 % CI: 1.53–2.38]) and adjustment disorders with depressive features (OR = 1.49 [95 % CI: 1.27–1.74]).</div></div><div><h3>Conclusions</h3><div>Our findings reveal significant associations between AU and various mental health disorders, particularly anxiety and personality disorders. These associations suggest a complex bidirectional relationship mediated through psychoneuroimmunological pathways involving the HPA axis, mast cell activation, and inflammatory cytokines. We recommend implementing specific screening tools (HADS, GAD-7) and a stepped-care approach for integrated dermatological and psychological management of AU patients.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101088"},"PeriodicalIF":3.5,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144864355","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":"Altered gut microbial diversity, composition, and metabolomic potential in patients with major depressive disorder and recent suicide attempt","authors":"Emese Prandovszky ,&nbsp;Hua Liu ,&nbsp;Emily G. Severance ,&nbsp;Victor W. Splan ,&nbsp;Faith B. Dickerson ,&nbsp;Robert H. Yolken","doi":"10.1016/j.bbih.2025.101081","DOIUrl":"10.1016/j.bbih.2025.101081","url":null,"abstract":"<div><div>This study investigates the role of the gut microbiome in suicidal behavior among individuals with major depressive disorder (MDD). Fecal samples from 50 hospitalized patients with MDD, including 35 with recent suicide attempts (60 % female) and 15 without a history of suicide (73 % female), were analyzed using 16S rRNA and shotgun sequencing to assess microbiome diversity and metabolic potential. Results revealed that suicide attempters exhibited significantly greater microbial richness and distinct beta-diversity patterns. Notably, they had higher levels of <em>Fenollaria timonensis</em> and lower levels of <em>Corynebacterium aurimucosum</em>. Additionally, 25 metabolic pathways differed between groups, with several linked to energy metabolism and amino acid processing—processes previously associated with MDD and suicidal behavior. These findings suggest that microbiome composition may influence suicide risk through gut-brain axis-mediated pathways, although due to the exploratory nature of this study further investigation is needed to validate our findings. Given the microbiome's modifiability, future research should explore microbial-targeted interventions as a potential strategy for suicide prevention in individuals with MDD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"48 ","pages":"Article 101081"},"PeriodicalIF":3.5,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852034","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}