Brain, behavior, & immunity - health最新文献

{"title":"Risk of neurodevelopmental disorders in the offspring of mothers with a history of endometriosis in Taiwanese women","authors":"Pei-Yin Yang ,&nbsp;Ching-Ming Wang ,&nbsp;Pei-Lun Liao ,&nbsp;Jing-Yang Huang ,&nbsp;Keng-Wei Liang ,&nbsp;Yu-Hsuan Lin ,&nbsp;Shun-Fa Yang ,&nbsp;Po-Hui Wang","doi":"10.1016/j.bbih.2025.101038","DOIUrl":"10.1016/j.bbih.2025.101038","url":null,"abstract":"<div><div>Several neurodevelopmental disorders have been linked to early life immune activation and inflammation, including developmental delay, cerebral palsy, intellectual disabilities, and other neurodevelopmental and psychiatric disorders. Certain inflammatory cytokines, such as interleukin-1β, interleukin-6, and tumor necrosis factor-α, secreted by endometriosis cells cause chronic pelvic inflammation and pain. The aim of this study was to evaluate whether maternal endometriosis increased the risk of neurodevelopmental disorders in offspring in <u>Taiwanese women</u>. The study included eligible mother–offspring pairs with maternal endometriosis (the case cohort) and mother–offspring pairs without maternal endometriosis (the comparison cohort) matched for maternal age at delivery, infant sex, and delivery date, both with offspring born during 2009–2016 and followed till 2019, from the Taiwan Maternal and Child Health Database. The incidence rates and crude hazard ratios (HRs) of development delay and cerebral palsy in the offspring delivered by mothers with endometriosis were higher than those in the offspring delivered by mothers without endometriosis (developmental delay: incidence 1.51 vs. 1.30 per 1000 person-months, crude HR = 1.16; cerebral palsy: incidence 0.04 vs. 0.03 per 1000 person-months, HR = 1.38). In model 1, the adjusted HRs of development delay and cerebral palsy in the offspring of mothers with endometriosis were 1.16 (95 % confidence interval [CI] = 1.11–1.22, <em>P</em> &lt; 0.0001) and 1.39 (95 % CI = 1.04–1.85, <em>P</em> = 0.0256). In model 2, these were 1.11 (95 % CI = 1.06–1.17) and 1.01 (95 % CI = 0.76–1.36), respectively. However, the HRs of intellectual disabilities and other neurodevelopmental and psychiatric disorders were not significantly different between the offspring of mothers with and without endometriosis. In conclusion, maternal endometriosis may increase the risks of cerebral palsy and specifically developmental delay in offspring.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101038"},"PeriodicalIF":3.7,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366147","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":"Dysregulated neural coding in the vagus nerve during long sepsis","authors":"Joshua J. Strohl ,&nbsp;Tomás S. Huerta ,&nbsp;Sergio Robbiati ,&nbsp;Patricio T. Huerta","doi":"10.1016/j.bbih.2025.101043","DOIUrl":"10.1016/j.bbih.2025.101043","url":null,"abstract":"<div><div>Sepsis is a life-threatening condition characterized by organ dysfunction resulting from the body's unbalanced and excessive response to an infection. ‘Long sepsis’ (LS) is an emerging concept referring to persistent sequelae experienced by long-term sepsis survivors, which include cognitive impairment, immune dysfunction, high cardiovascular risk, fatigue, and depression. Here, we investigated the role of the vagus nerve, a key component of the inflammatory reflex, in a mouse model of LS. Six weeks after cecal ligation and puncture (CLP) or sham surgery, we performed electrophysiological recordings from the cervical vagus nerve in anesthetized male mice. We found that LS mice exhibited significantly higher baseline vagal activity compared to controls, with elevated firing rates during both respiratory bursts and inter-burst intervals. Control mice showed clear increases in vagal activity following systemic administration of pro-inflammatory cytokines, tumor necrosis factor (TNF) and interleukin-1β (IL-1β), but LS mice displayed markedly dysregulated responses. LS mice showed altered firing dynamics, with many vagal units decreasing rather than increasing their activity after cytokine stimulation. Using a naïve Bayes decoder, we demonstrated that LS disrupted the neural code in the vagus nerve, significantly altering its activity pattern in response to cytokine signals. These results suggest that LS fundamentally alters vagus nerve function, with elevated baseline activity and diminished responsiveness to inflammatory signals. This neurophysiological dysregulation may contribute to the persistent multi-organ dysfunctions observed in long sepsis survivors, suggesting a potential role for vagal signaling in sepsis outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101043"},"PeriodicalIF":3.7,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144335643","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":"Autoantibody profiling of autism spectrum disorder patients with monoamine oxidase a deficiency","authors":"Guan-Da Syu ,&nbsp;Yawei Cheng ,&nbsp;Kevin Chen ,&nbsp;Chih-Yung Yang ,&nbsp;F.X. Reymond Sutandy ,&nbsp;Chia-Chien Liu ,&nbsp;Chien-Sheng Chen ,&nbsp;Jean C. Shih","doi":"10.1016/j.bbih.2025.101039","DOIUrl":"10.1016/j.bbih.2025.101039","url":null,"abstract":"<div><div>Monoamine oxidase A (MAO A) is a key enzyme for serotonin metabolism. Knockout MAO A in mice results in elevated serotonin, altered serum autoantibodies, and autistic-like behavior. There is a subset of patients with autism spectrum disorder (ASD) who exhibit hyperserotonemia. The link between the MAO A, hyperserotonemia, immunity, and ASD is still unknown. To address this question, we harness the high-density human proteome microarray to profile the serum autoantibodies in ASD patients with or without MAO A deficiency. We recruited 25 subjects, including 20 ASD patients, from National Yang Ming Chiao Tung University Hospital and determined their plasma serotonin levels, screened for MAO A gene mutations and identified one patient with a C374 G mutation, which abolished MAO A activity and showed the highest serotonin level (hsASD; 518.42 ng/ml) and severe ASD symptoms. In another family with twin brothers, one was diagnosed with mild ASD and exhibited an increased serotonin level (isASD; 31.48 ng/ml), while the other twin was a healthy control. These three subjects were used for serum autoantibody profiling using high-density human proteome microarrays. Comparing serum antibodies from hsASD with healthy control, we identified 354 up-regulated and 398 down-regulated autoantibodies in hsASD. By comparing isASD with healthy controls, we reported 235 up-regulated and 279 down-regulated autoantibodies in isASD. Interestingly, the up-regulated autoantibodies for hsASD were enriched in the brain region and exhibited distinct features from that of isASD. This study indicates that MAO A deficiency and serotonin levels significantly impact the immunological changes in ASD patients, which may shed some light on pathological mechanisms and provide potential biomarkers for translational research in ASD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101039"},"PeriodicalIF":3.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366053","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":"Where's my mom? Resilient maternal preference in post-weaning male and female mice within a multi-chamber social behavior task","authors":"Maggie M. Slamin ,&nbsp;Indra R. Bishnoi ,&nbsp;Izabella M. Bankowski,&nbsp;Haley A. Norris,&nbsp;Evan A. Bordt","doi":"10.1016/j.bbih.2025.101034","DOIUrl":"10.1016/j.bbih.2025.101034","url":null,"abstract":"<div><div>One of the earliest and most important social bonds for many mammals is the bond formed with their mother. Mothers often provide essential benefits for offspring development and survival. Growing evidence suggests that this social bond is retained even when animals gain independence, such as during the juvenile period immediately following weaning. Here, we investigated whether or not juvenile mice (postnatal day [P]26) retain the ability to recognize and prefer their mothers post-weaning. We further investigated the strength of this bond using an acute immune activator. On P26, male and female C57BL/6J mice were intraperitoneally injected with the endotoxin lipopolysaccharide (LPS) or saline control (0.5 mg/kg). Four hours later, mice were subject to a five-chamber social preference task (the AGORA) containing their biological mother, a sex- and age-matched novel mouse, a sex- and age-matched sibling, a novel object, and an empty chamber. Our findings reveal that juvenile mice exhibit a strong maternal preference, which was significantly greater than chance and higher compared to any other social or non-social stimuli. While LPS exposure reduced the time spent investigating all stimuli, juvenile maternal preference was not significantly altered by LPS exposure. These effects were especially pronounced in females, while subtle shifts towards novel exploration began to emerge in males by P26. The novel multi-chamber task employed in the present study offered a more nuanced understanding of how social bonds evolve and vary across sex. The current findings suggest that juvenile mice have a robust social preference for their mother that is resilient to early-life immune activation.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101034"},"PeriodicalIF":3.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144335644","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":"Mediating role of Interleukin-6 in the predictive association of diabetes with Hippocampus atrophy, Amyloid, Tau, and Neurofilament pathology at pre-clinical stages of diabetes-related cognitive impairment","authors":"Asma Hallab ,&nbsp;The Health and Aging Brain Study (HABS-HD) Study Team","doi":"10.1016/j.bbih.2025.101031","DOIUrl":"10.1016/j.bbih.2025.101031","url":null,"abstract":"<div><h3>Introduction</h3><div>Type-2 diabetes (T₂DM) has been associated with higher dementia risks, but the mechanisms are still unclear, and there is increasing evidence of the role of cytokines. Interleukin-6 (IL-6) mediating effect has never been explored.</div></div><div><h3>Methods</h3><div>The study included a subset of 1927 community-dwelling participants from the Health and Aging Brain Study: Healthy Disparities (HABS-HD) cohort with complete data. Cross-sectional and longitudinal analyses were performed. Associations were studied using multivariable linear, logistic, and mediation analysis with non-parametric bootstrapping.</div></div><div><h3>Results</h3><div>T₂DM and IL-6 were associated with worse executive function, Hippocampus atrophy, lower Aß₄₂/Aß₄₀ ratio, and higher Aß₄₀, Aß₄₂, total Tau, and NfL levels. IL-6 mediated 5 % of the association of T₂DM with Aß₄₀ ([1.5 %–10 %], <em>p-</em>value&lt;2 × 10⁻¹⁶), 4 % with Aß₄₂ ([0.7 %–11 %], <em>p-</em>value = 0.014), 8 % with TMT-B ([0.2 %–35 %], <em>p-</em>value = 0.046), 11 % with total Tau ([2.5 %–40 %], <em>p-</em>value = 0.010), 5 % with NfL ([1.6 %–8 %], <em>p-</em>value&lt;2 × 10⁻¹⁶), and 12 % Hippocampus atrophy ([3 %–49 %], <em>p-</em>value = 0.004). The results, except TMT-B, were replicated in the longitudinal analysis of long-lasting T₂DM on non-previously diagnosed cognitive impairment.</div></div><div><h3>Conclusions</h3><div>The study captured a pre-clinical stage of the T₂DM-dementia association. The mediating effect of IL-6 is a novelty that has to be further explored and accounted for in risk stratification and preventive measures, particularly in ethnic minorities.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101031"},"PeriodicalIF":3.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330560","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":"Targeting the P2X7 receptor signaling pathway: Unlocking therapeutic strategies for autism spectrum disorder","authors":"Chetana Ahire,&nbsp;Ginpreet Kaur","doi":"10.1016/j.bbih.2025.101037","DOIUrl":"10.1016/j.bbih.2025.101037","url":null,"abstract":"<div><div>Autism spectrum disorder (ASD) is a common developmental neurological disorder that has a significant genetic predisposition and is marked by an early beginning of impairment of social communication and restricted repetitive behaviors, as well as loss of interest in activities. Though it is a common condition, pathogenetic mechanisms and etiologic foundations are still unclear; diagnostic strategies and treatments remain inadequate and restricted. Hence, there is an ongoing need to develop safer and more effective therapeutic strategies. Recent findings indicate P2X7 receptor upregulation plays a key role in ASD development through multiple pathological mechanisms, including maternal immune activation, mitochondrial dysfunctioning, oxidative stress, and neuroinflammation. When ATP from outside the cell attaches to P2X7 receptors, it opens channels that let sodium, calcium, and potassium flow in and out of the cell. Long-term receptor stimulation generates large pores in the membrane, potentially facilitating apoptotic and inflammatory mechanisms. So, based on studies using drugs that block the P2X7 receptor and genetic methods, stopping the P2X7 receptor appears to improve the harmful effects related to ASD. So, the therapeutic lead is the brain-permeable P2X7 receptor antagonists that deserve more complete clinical validation.</div><div>This review discusses how the P2X7 receptor is involved in the development of ASD and looks at possible drug strategies to slow down the disease.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101037"},"PeriodicalIF":3.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144314658","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":"Prevalence of the anti-CASPR2 autoantibody in patients with somatic symptom disorder accompanied by medically unexplained pain","authors":"Shingo Katayama ,&nbsp;Gayatri Nayanar ,&nbsp;Takayuki Suga ,&nbsp;Motoko Watanabe ,&nbsp;Chihiro Takao ,&nbsp;Yojiro Umezaki ,&nbsp;Hidehiko Takahashi ,&nbsp;Akira Toyofuku ,&nbsp;Hiroki Shiwaku","doi":"10.1016/j.bbih.2025.101036","DOIUrl":"10.1016/j.bbih.2025.101036","url":null,"abstract":"<div><h3>Background</h3><div>Medically unexplained symptoms (MUS) with pain are classified as somatic symptom disorder (SSD) with pain in the field of psychiatry, although an undetected biological basis may underlie at least some of these cases. One such candidate etiology is autoantibodies. Autoantibody etiologies are suspected in MUS with pain, including fibromyalgia, which is highly related to SSD accompanied with pain. Furthermore, autoantibodies against contactin-associated protein-like 2 (CASPR2) are known to induce neuropathy and pain, yet no study has examined the prevalence or clinical significance of anti-CASPR2 autoantibodies in patients with SSD accompanied with pain. Thus, the current study aims to investigate the seroprevalence of the anti-CASPR2 autoantibody among patients with SSD accompanied with pain and their associations with disease characteristics.</div></div><div><h3>Methods</h3><div>The serum samples obtained from 264 patients with SSD accompanied with pain and 260 healthy controls were screened for anti-CASPR2 autoantibodies using a cell-based assay. Among the 264 patients enrolled, 231 with oral dysesthesia (including oral cenesthopathy) were assessed for clinical symptom severity using the Visual Analog Scale (VAS), Pain Catastrophizing Scale (PCS), and Somatic Symptom Scale-8 (SSS-8).</div></div><div><h3>Results</h3><div>Of the 264 patients, 18 (6.8 %) tested seropositive for anti-CASPR2 autoantibodies. Among the 231 patients with oral dysesthesia, 12 (5.4 %) were positive for anti-CASPR2 autoantibodies. These patients with oral dysesthesia who were positive for anti-CASPR2 autoantibody reported significantly higher SSS-8 scores than those who were negative for autoantibody.</div></div><div><h3>Conclusion</h3><div>Among patients with SSD accompanied with medically unexplained pain, a small subgroup was seropositive for anti-CASPR2 autoantibodies.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101036"},"PeriodicalIF":3.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144297292","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":"Olfactory impairment associated with reduced physical capacity 24 months after COVID-19","authors":"Christoffer Granvik ,&nbsp;Alicia Lind ,&nbsp;Guilherme W.F. Barros ,&nbsp;Clas Ahlm ,&nbsp;Sara Anderson ,&nbsp;Linus Andersson ,&nbsp;Johan Normark","doi":"10.1016/j.bbih.2025.101032","DOIUrl":"10.1016/j.bbih.2025.101032","url":null,"abstract":"<div><h3>Background</h3><div>Olfactory impairment has been associated with adverse health outcomes, particularly in older populations, including cognitive decline, malnutrition, and frailty. The COVID-19 pandemic highlighted olfactory impairment as a key symptom affecting individuals across all age groups, raising concerns about its long-term impacts. This study investigates the association between post-acute olfactory impairment and long-term physical capacity in COVID-19 patients, hypothesizing that impaired olfaction is linked to reduced physical performance.</div></div><div><h3>Methods</h3><div>This prospective cohort study included 63 hospitalized and non-hospitalized COVID-19 patients (38.1 % women; median age 51 years, IQR 47.0–60.0) who underwent olfactory testing 1–3 months post-infection. Olfactory assessments included threshold screening, supra-threshold intensity ratings, and an odour identification test. Physical capacity was assessed using the 1-min sit-to-stand test at follow-ups (3, 6, 12, and 24 months). Partial correlation analysis and linear mixed models were used to analyse the data, adjusting for covariates such as age, sex, BMI, comorbidities, smoking status, and severity of infection.</div></div><div><h3>Results</h3><div>In the early post-acute phase, 36.5 % of participants exhibited olfactory impairment. We identified a significant, negative correlation between objectively tested olfactory impairment and physical capacity at all follow-ups. In a linear mixed model adjusted for relevant covariates, olfactory impairment was associated with reduced physical capacity up to 24 months after infection. The association strengthened over time, reflected by the increasing beta values for the interaction term: 0.09 (p = 0.200) at 6 months, 0.13 (p = 0.053) at 12 months, and 0.23 (p = 0.001) at 24 months.</div></div><div><h3>Conclusion</h3><div>Individuals with olfactory impairment in the early post-acute phase of COVID-19 infection were more likely to exhibit diminished physical capacity 24 months later. This study highlights the broader implications of olfactory impairment, previously noted mainly in older populations, demonstrating its relevance across age groups. The COVID-19 pandemic presented a unique opportunity to investigate this relationship, enhancing our understanding of how olfactory impairments relate to long-term physical performance. These findings emphasize the need for further research with larger, more diverse cohorts and objective longitudinal assessments to confirm and extend these observations.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101032"},"PeriodicalIF":3.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307682","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":"Physical exercise to rebalance kynurenine metabolism in borderline personality disorder – Preliminary findings","authors":"F. Javelle ,&nbsp;W. Bloch ,&nbsp;K. Koppe ,&nbsp;S. Krombholz ,&nbsp;M. Thevis ,&nbsp;L. Wanka ,&nbsp;H. Zoche ,&nbsp;A. Philipsen ,&nbsp;A. Mehren","doi":"10.1016/j.bbih.2025.101030","DOIUrl":"10.1016/j.bbih.2025.101030","url":null,"abstract":"<div><div>Systemic inflammation and dysregulated kynurenine (KYN) metabolism are increasingly recognised as key factors in various psychiatric disorders. Imbalances in the KYN pathway are associated with psychological and cognitive symptoms across disorders like depression and schizophrenia, yet remain unexplored in borderline personality disorder (BPD). This study is the first to compare KYN metabolism together with the myokine IL-6 in BPD patients and healthy controls and to examine acute exercise effects on this pathway in BPD. Fourteen patients with BPD and nine controls participated in two experimental conditions: cycling exercise and a control session. Serum samples were analysed for tryptophan (TRP), KYN, kynurenic acid (KA), and quinolinic acid (QA). Results revealed greater QA/KYN and lower KA/KYN and KA/QA ratios in BPD, indicating a shift toward the neurotoxic branch. Acute exercise increased KA, KA/KYN, KA/QA, and IL-6 levels, highlighting its potential to enhance neuroprotective KYN activity. These findings suggest KYN pathway dysregulation in BPD and support physical exercise as a promising intervention to rebalance this pathway. Further research should investigate long-term exercise effects and their impact on psychological outcomes in BPD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101030"},"PeriodicalIF":3.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279822","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":"Peripheral blood transcriptomic differences predict depression status in individuals undergoing bariatric surgery","authors":"Rebecca Milton ,&nbsp;Anna P. McLaughlin ,&nbsp;Nicole Mariani ,&nbsp;Melisa Kose ,&nbsp;Zuzanna Zajkowska ,&nbsp;Giulia Lombardo ,&nbsp;Naghmeh Nikkheslat ,&nbsp;Esperanza Perucha ,&nbsp;Valeria Mondelli","doi":"10.1016/j.bbih.2025.101029","DOIUrl":"10.1016/j.bbih.2025.101029","url":null,"abstract":"<div><div>More than one third of candidates for bariatric surgery suffer with clinical depression. Significant reduction in depression following bariatric surgery has been shown, but this is not consistent for all patients. The biological mechanisms behind the association between obesity and depression and behind persistent/remitted depression post-surgery remain unclear. This study aimed to identify potential biological mechanisms involved in this association. As part of the longitudinal observational bariatric surgery and depression (BARIDEP) study, blood samples were collected from individuals prior to bariatric surgery. For this study we selected n = 29 subjects (from the original sample of n = 85 participants) based on their Hamilton Depression (HAM-D) scale scores at baseline and at 6 months post-surgery and grouped them as controls (n = 10), persistent depression (n = 7) or remission (n = 12). Participants were selected to be matched for age, sex and BMI. RNA was extracted and bulk RNAseq was performed. Data were analysed for differential expression and gene set enrichment across the 3 groups of interest. Analysis of the differential gene expression showed seven genes differentially expressed across the three groups, with genes mainly involved in immune activation or synaptic function. The greatest differences were found between the persistent and remitting depression groups, despite both experiencing clinical depression at the time of sample collection. Our data show distinct baseline gene expression and gene enrichment suggesting different immune and metabolic mechanisms possibly involved in persistent vs remitting depression post-bariatric surgery.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"47 ","pages":"Article 101029"},"PeriodicalIF":3.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279777","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}