Brain, behavior, & immunity - health最新文献

{"title":"HIV and Low Omega-3 Levels May Heighten Hippocampal Volume Differences Between Men and Women With Substance Use","authors":"Hong Lai ,&nbsp;Jiachen Zhuo ,&nbsp;Glenn Treisman ,&nbsp;Gary Gerstenblith ,&nbsp;David D. Celentano ,&nbsp;Yihong Yang ,&nbsp;Betty Jo Salmeron ,&nbsp;Hong Gu ,&nbsp;Thorsten M. Leucker ,&nbsp;Xiao Liang ,&nbsp;Raul N. Mandler ,&nbsp;Jag Khalsa ,&nbsp;Óscar Peña-Nogales ,&nbsp;Shaoguang Chen ,&nbsp;Shenghan Lai ,&nbsp;Elana Rosenthal ,&nbsp;Karl Goodkin ,&nbsp;Vincent A. Magnotta","doi":"10.1016/j.bbih.2025.100988","DOIUrl":"10.1016/j.bbih.2025.100988","url":null,"abstract":"<div><h3>Background</h3><div>Sex differences in hippocampal volumes are well-documented, but their interaction with HIV status and omega-3 fatty acids—particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—remains unclear, especially in underserved populations. This study examines how HIV and omega-3 fatty acids influence sex differences in hippocampal volume and explores whether cognitive performance related to episodic memory modifies the association of omega-3 levels with hippocampal volume, considering both HIV status and sex.</div></div><div><h3>Methods</h3><div>We enrolled 166 participants aged over 45 years from a Baltimore, Maryland cohort. Brain MRIs were performed using a 3.0-T Siemens scanner, and volumetric segmentation was conducted with FreeSurfer (version 6.0), adjusting for intracranial volume (ICV).</div></div><div><h3>Results</h3><div>Our study found that: (1) Among HIV-negative participants, females had significantly lower hippocampal volumes than males in 1 of 26 regions, whereas HIV-positive females had lower volumes in 13 of 26 regions (p &lt; 0.006 for HIV-negative vs. HIV-positive females), (2) In HIV-positive individuals with EPA levels ≤0.40 %, females exhibited lower volumes in 11 of 26 regions, compared to no differences in those with EPA levels &gt;0.40 % (p = 0.0003 for ≤0.40 % vs. &gt;0.40 %), (3) Across all participants, lower EPA and DHA levels were associated with greater sex differences in hippocampal volumes, which diminished or disappeared at higher EPA and DHA levels (p &lt; 0.00001 for EPA ≤0.40 % vs. &gt;0.40 %; p = 0.004 for DHA ≤2.0 % vs. &gt;2.0 %), and (4) Among Adults with lower episodic memory, higher log-scaled EPA levels were independently associated with greater hippocampal volume.</div></div><div><h3>Conclusions</h3><div>HIV may amplify sex differences in hippocampal volumes, disproportionately affecting females. Higher EPA and DHA levels may mitigate these effects, suggesting a protective role against hippocampal atrophy. Further studies are warranted to confirm these findings and explore whether the benefits extend to males with HIV or individuals without HIV.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100988"},"PeriodicalIF":3.7,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799193","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":"Cardiovascular health and its association with dementia, Parkinson's Disease, and mortality among UK older adults","authors":"Michael F. Georgescu ,&nbsp;May A. Beydoun ,&nbsp;Jordan Weiss ,&nbsp;Jagdish Kubchandani ,&nbsp;Sri Banerjee ,&nbsp;Alyssa A. Gamaldo ,&nbsp;Michele K. Evans ,&nbsp;Alan B. Zonderman","doi":"10.1016/j.bbih.2025.100986","DOIUrl":"10.1016/j.bbih.2025.100986","url":null,"abstract":"<div><h3>Background</h3><div>Previous research has primarily examined individual factors of cardiovascular health (CVH) and disease in PD and dementia, but no study has examined CVH measures with PD, dementia, and mortality simultaneously while accounting for potentially confounding factors.</div></div><div><h3>Objectives</h3><div>To examine the relationship between CVH, all-cause dementia, Parkinson's disease (PD), and mortality, focusing on associations and health transitions from a large population-based study.</div></div><div><h3>Methods</h3><div>We investigated these relationships using Cox Proportional Hazards and multistate parametric models with Weibull regression from the UK Biobank data (n = 269,816, Age = 50 + y individuals, ≤15y follow-up, 2006–2021).</div></div><div><h3>Results</h3><div>Full Cox models found poor CVH (measured with standardized reverse-coded Life's Essential 8 total score, LE8_zrev), to be associated with increased risks for all-cause dementia (Hazard Ratio (HR) = 1.14, 95 % CI: 1.11–1.18, P &lt; 0.001) and all-cause mortality (HR = 1.31, 95 % CI: 1.29–1.33, P &lt; 0.001). Unlike “Healthy to PD” and “Dementia→Death” transitions, PD→Death (Weibull full model: HR = 1.18, 95 % CI: 1.06–1.31, P = 0.002), Healthy→dementia (HR = 1.15, 95 % CI: 1.12–1.19, P &lt; 0.001), and Healthy→Death (HR = 1.33, 95 % CI: 1.32–1.35, P &lt; 0.001) exhibited a positive relationship with poor CVH.</div></div><div><h3>Conclusions</h3><div>Poor CVH is directly associated with an increased risk of mortality from PD, transition into Dementia, and all-cause mortality without dementia or PD occurrence. Clinicians should aggressively screen for and manage CVH risk measures to reduce the risk of poor cognitive health outcomes.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100986"},"PeriodicalIF":3.7,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143747663","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":"Smoking disrupts the relationship between cerebrospinal fluid IL-1β and multiple subdimensions of sleep","authors":"Yueling Hu ,&nbsp;Siyuan Li ,&nbsp;Yingjie Chen ,&nbsp;Xingguang Luo ,&nbsp;Yu-Hsin Chen ,&nbsp;Yimin Kang ,&nbsp;Weiming Hu ,&nbsp;Li Chen ,&nbsp;Siling Ye ,&nbsp;Xinchen Zhou ,&nbsp;Yanlong Liu ,&nbsp;Fan Wang ,&nbsp;Yuying Li","doi":"10.1016/j.bbih.2025.100987","DOIUrl":"10.1016/j.bbih.2025.100987","url":null,"abstract":"<div><h3>Objective</h3><div>Inflammatory factors and cigarette smoking have been associated with sleep disorders but molecular mechanisms that regulate sleep, specifically the role of interleukin-1β (IL-1β), remain controversial. Individuals’ cerebrospinal fluid (CSF) IL-1β, smoking behavior, and sleep data were collected to investigate how smoking may influence the relationship between CSF IL-1β and sleep via moderation analysis.</div></div><div><h3>Methods</h3><div>A total of 191 Chinese male patients, including 104 non-smokers and 87 active smokers, scheduled for anterior cruciate ligament reconstructive surgery, were recruited. Pittsburgh Sleep Quality Index (PSQI) scores were collected prior to surgery, and CSF samples were obtained during preoperative lumbar puncture.</div></div><div><h3>Results</h3><div>Active smokers compared to non-smokers exhibited higher scores across various subdimensions of PSQI, specifically poorer sleep quality, increased sleep latency, reduced sleep efficiency, and heightened sleep disturbance (all p &lt; 0.05). Positive correlations were observed between CSF IL-1β levels and PSQI total scores, as well as several subdimensions of sleep (all p &lt; 0.05) in non-smokers. In contrast, a negative correlation was observed between CSF IL-1β levels and sleep efficiency scores (p &lt; 0.05) among active smokers. Moderation analysis revealed that smoking negatively moderated the relationship between CSF IL-1β and sleep, particularly in PSQI total scores (β = −0.95, p &lt; 0.001), sleep latency scores (β = −1.05, p &lt; 0.001), and sleep disturbance scores (β = −0.45, p &lt; 0.05).</div></div><div><h3>Conclusions</h3><div>The current study found that smoking disrupts multiple subdimensions of sleep and moderates the effect of the neuroinflammatory factor CSF IL-1β on PSQI sleep latency and sleep disturbance scores.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100987"},"PeriodicalIF":3.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143760773","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":"SARS-CoV-2-induced sensory perturbations: A narrative review of clinical phenotypes, molecular pathologies, and possible interventions","authors":"Randal A. Serafini ,&nbsp;Justin J. Frere ,&nbsp;Ilinca M. Giosan ,&nbsp;Chinwe A. Nwaneshiudu","doi":"10.1016/j.bbih.2025.100983","DOIUrl":"10.1016/j.bbih.2025.100983","url":null,"abstract":"<div><h3>Background</h3><div>The acute and post-acute sequelae of SARS-CoV-2 infection have been of great clinical interest since the inception of the COVID-19 pandemic. Despite a high prevalence of individuals with persistent symptoms, a wholistic view of the effects of SARS-CoV-2 on special sensory systems is lacking. Considering the significant impact of normal sensory function on quality of life, the goal of this review is to highlight unresolved issues related to SARS-CoV-2-associated insults to the sensory nervous system.</div></div><div><h3>Major findings</h3><div>In this narrative review, we discuss the epidemiology of SARS-CoV-2-induced sensory perturbations, underlying pathological mechanisms, and possible therapeutic strategies across the olfactory, gustatory, somatosensory, visual, and auditory systems. Examined literature included studies with human biospecimens, human-derived cell lines, and naturally susceptible animal models, which highlighted evidence of persistent functional disruption in all sensory systems. SARS-CoV-2 infection was associated with persistent inflammation in the olfactory epithelium/bulb, somatosensory ganglia, and gustatory systems, long-term transcriptional perturbations in the sensory central nervous system and peripheral nervous system, and detectable degeneration/apoptosis in the gustatory and visual systems. Few studies have proposed evidence-based therapeutic strategies for attenuating specific sensory abnormalities after SARS-CoV-2 infection.</div></div><div><h3>Conclusion</h3><div>While the olfactory system, and to some extent the visual and somatosensory systems, have been more thoroughly investigated from symptomatology, behavioral and molecular perspectives, there is still an unmet need for the development of therapeutics to treat COVID-induced impairment of these systems. Further, additional attention must be placed on COVID-associated impairment of the gustatory, visual, and auditory systems, which lack detailed mechanistic investigations into their pathogenesis.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100983"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143724314","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":"Predictors of fatigue progression in long COVID among young people","authors":"Elias Myrstad Brodwall ,&nbsp;Joel Selvakumar ,&nbsp;Lise Beier Havdal ,&nbsp;Silke Sommen ,&nbsp;Lise Lund Berven ,&nbsp;Erin Cvejic ,&nbsp;Vegard Bruun Bratholm Wyller ,&nbsp;Maria Pedersen","doi":"10.1016/j.bbih.2025.100982","DOIUrl":"10.1016/j.bbih.2025.100982","url":null,"abstract":"<div><div>Long COVID, or post-COVID-19 condition (PCC), has emerged as a significant health concern, with fatigue being the most prevalent persistent symptom among young people. However, research on predictors of fatigue progression in young populations is limited. This study aimed to investigate factors during acute SARS-CoV-2 infection that could predict fatigue progression between six and 12 months post-infection in a cohort of young people with chronic fatigue following COVID-19. Data from the Long-Term Effects of COVID-19 in Adolescents (LoTECA) project were analyzed. A total of 93 participants (mean age 18.5 years, 84 % female) with chronic fatigue at six months, completed the 12-month follow-up. Multivariate analyses identified non-European ethnicity, higher interferon gamma (IFN-γ) levels, and lower RR-interval (higher resting heart rate) during acute infection as significant predictors of fatigue progression from six to 12 months. These three factors explained 21 % of the variance in the fatigue score, highlighting the importance of ethnicity, immune response, and autonomic function in the trajectory of long COVID fatigue. Early identification and targeted interventions, particularly for ethnic minorities and those with specific immune or autonomic markers during acute infection, may be helpful in reducing long-term fatigue. Further research is needed to explore treatment strategies for affected young populations.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100982"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697250","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":"Temporal dynamics of inflammatory, platelet, and neurotrophic markers during social stress in relation to suicidal ideation and suicide attempt history","authors":"Aiste Lengvenyte ,&nbsp;Emilie Olié ,&nbsp;Fabrice Cognasse ,&nbsp;Hind Hamzeh-Cognassse ,&nbsp;Adrian Alacreu-Crespo ,&nbsp;Philippe Courtet","doi":"10.1016/j.bbih.2025.100984","DOIUrl":"10.1016/j.bbih.2025.100984","url":null,"abstract":"<div><div>Interpersonal stress is a major precipitant of suicidal ideation (SI) and suicide attempts (SA), yet the underlying biological mechanisms remain unclear. This study examined dynamic plasma concentrations of inflammatory, platelet activation, and neurotrophic markers during acute social stress in 76 depressed women (mean age: 39.7 ± 1.39 years) with and without SA history or recent SI. Participants underwent the Trier Social Stress Test, with biomarkers measured at five time points before, during, and after the stressor. Covariate-adjusted growth curve models and area under the curve analyses were applied. SI was associated with elevated overall TNF-α levels (0.82 ± 0.05 vs. 0.61 ± 0.05, p = 0.039). Participants without SI showed cubic trajectories in TNF-α (t₂₂₈ = 4.76, p &lt; 0.001) and MIP-1β (t₂₃₅ = 2.12, p = 0.035), and quadratic trajectories in platelet markers TSP-1 (t₂₇₄ = −2.42, p = 0.016), PF-4 (t₂₇₄ = −2.25, p = 0.025), and NAP-2 (t₂₇₄ = −2.43, p = 0.016), which were absent in participants with SI. Cubic patters in inflammatory responses were also observed in participants without SA history, but not in suicide attempters (TNF-α: t₂₂₈ = 3.15, p = 0.030; MIP-1β: t₂₃₅ = 2.74, p = 0.007). Meanwhile, participants with SI or SA, but not those without, showed a linear BDNF increase (t₂₇₅ = 2.39, p = 0.017; t₂₇₅ = 2.28, p = 0.024, respectively). These findings suggest that SI and SA may be associated with impaired dynamic immune-inflammatory, platelet, and neurotrophic systems responses to acute interpersonal stress, reflecting systemic biological rigidity.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100984"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143695921","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":"A case of MOGAD with rectal adenocarcinoma: Comorbidity or paraneoplastic neurological syndrome?","authors":"Yiyi Luo ,&nbsp;Gang Peng ,&nbsp;Jiahua Liang ,&nbsp;Xuwei Song ,&nbsp;Jiayu Tang","doi":"10.1016/j.bbih.2025.100985","DOIUrl":"10.1016/j.bbih.2025.100985","url":null,"abstract":"<div><h3>Background</h3><div>Myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare autoimmune disease characterized primarily by central nervous system demyelination. We report a rare case of MOGAD coexisting with rectal adenocarcinoma.</div></div><div><h3>Case report</h3><div>A 59-year-old female presented with fever and bilateral lower limb weakness. MRI of the brain revealed abnormal signals in multiple regions of the cerebrum, brainstem, and spinal cord. Both serum and cerebrospinal fluid tested positive for MOG antibodies. The symptoms improved after steroid therapy. During hospitalization, colonoscopy and pathological examination revealed rectal cancer, which was subsequently treated surgically. After six months of follow-up, neither the tumor nor MOGAD recurred.</div></div><div><h3>Conclusion</h3><div>Paraneoplastic etiologies may also contribute to the development of MOGAD. To date, no cases of MOGAD associated with rectal cancer have been reported. It remains uncertain whether paraneoplastic neurologic syndrome (PNS) is involved in this patient.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100985"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143724315","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 inflammation in the development of tic symptoms in subjects with ADHD","authors":"Nagahide Takahashi ,&nbsp;Hidekazu Kato ,&nbsp;Yoshihiro Nawa ,&nbsp;Shiori Ogawa ,&nbsp;Kenji J. Tsuchiya ,&nbsp;Takashi Okada","doi":"10.1016/j.bbih.2025.100981","DOIUrl":"10.1016/j.bbih.2025.100981","url":null,"abstract":"<div><div>Tourette's syndrome is characterized by multiple motor and 1 or more vocal tics that persist for more than 1 year since first tic onset. It is well known that subjects with Tourette's syndrome show varieties of comorbidities, and ADHD is one of the most prevalent comorbid symptoms. In most cases, ADHD symptoms is known to precede the onset of tic symptoms, but how subjects with ADHD develop Tourette's syndrome later in life remains unclear.</div><div>Both Tourette's syndrome and ADHD is highly heritable, and genome wide association studies of ADHD and Tourette's syndrome showed that Tourette's syndrome and ADHD are genetically related. In order to identify the factor to cause tic symptoms in subjects with ADHD, we conducted two-sample mendelian randomization analysis, gene-set analysis and identified <em>neutrophil degranulation</em> is a pathways specific to Tourette's syndrome. Molecular analysis showed that Neutrophil-lymphocyte ratio may be relatively upregulated within the normal range in subjects with ADHD and Tourette's syndrome compared to subjects with ADHD only.</div><div>As the molecular analysis is still in its preliminary stages, the current results suggest that inflammation may be a contributing factor in the development of symptoms of Tourette's syndrome in subjects with ADHD. If these results can be replicated, neutrophil-lymphocyte ratio could serve as a potential a biomarker for the risk of Tourette's syndrome.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100981"},"PeriodicalIF":3.7,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143725726","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":"Maternal mental health disorders associate with their child's asthma: A register-based study","authors":"Eetu P. Kanerva ,&nbsp;Minna M. Lukkarinen ,&nbsp;Marika H. Leppänen ,&nbsp;Bernd K. Pape ,&nbsp;Päivi T.K. Rautava ,&nbsp;Max R.J. Karukivi","doi":"10.1016/j.bbih.2025.100979","DOIUrl":"10.1016/j.bbih.2025.100979","url":null,"abstract":"<div><h3>Background</h3><div>Maternal perinatal mental health disorders contribute to the development of their child's asthma. We investigated the associations between maternal mental health disorders one year before and three years after childbirth to their child's non-allergic asthma and allergic asthma.</div></div><div><h3>Methods</h3><div>From 310701 children born in Finland from 2001 to 2006 and their 232240 mothers, health care registers were collected. Using the International Classification of Diseases 10th revision, a maternal mental health disorder was defined as any mental or behavioral disorder diagnosis (F00−99) from the one year before and three years after childbirth. The outcome was their child's asthma diagnosis (e.g., J45, J45.0, J45.1, J45.8, J45.9, or J46.0) at 7–12 years divided into allergic (J45.0) and non-allergic (J45.1) asthma.</div></div><div><h3>Results</h3><div>Of the children, 19000 (6.1 %) were diagnosed with asthma and 12953 (5.6 %) of the mothers with a mental health disorder. The child's asthma was associated with a maternal mental health disorder (adjusted odds ratio 1.24; 95 % confidence interval 1.16−1.33), smoking during pregnancy (1.08; 1.03−1.13), asthma history (2.94; 2.82−3.06), the mother having a production <em>vs</em>. higher management/executive occupational role (1.16; 1.10−1.23), or the child being male (1.47; 1.42−1.52), all <em>p</em> <em>&lt;</em> .001. Maternal mental health disorders were associated more with their child's non-allergic asthma (1.37; 1.18−1.60) than allergic asthma (1.17; 1.05−1.30), both <em>p</em> <em>&lt;</em> .001.</div></div><div><h3>Conclusions</h3><div>Maternal mental health disorders perinatally and during the early life of their child were associated with their child's asthma supporting intrauterine and early-life programming on the effects of maternal mental health on their child's respiratory morbidity risk.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100979"},"PeriodicalIF":3.7,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697319","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":"Oral microbiome composition is associated with depressive symptoms during pregnancy","authors":"Oryan Agranyoni ,&nbsp;Treva Rowley ,&nbsp;Sara B. Johnson ,&nbsp;Heather Volk ,&nbsp;William Schleif ,&nbsp;Raquel G. Hernandez ,&nbsp;Lauren M. Klein ,&nbsp;Robert H. Yolken ,&nbsp;Sarven Sabunciyan","doi":"10.1016/j.bbih.2025.100978","DOIUrl":"10.1016/j.bbih.2025.100978","url":null,"abstract":"<div><h3>Background</h3><div>Oral microbiome dysbiosis has been linked to systemic disease with an underlying inflammatory etiology. However, the possible association of the oral microbiome in antenatal depression has received little attention.</div></div><div><h3>Methods</h3><div>Participants were pregnant women in the PREDICT prenatal cohort study (n = 400) who provided saliva during pregnancy. Using 16S rRNA sequencing, we determined the association between composition of the salivary microbiome and a continuous measure of depressive symptoms (Center for Epidemiological Studies-Depression Scale (CES-D): 0–60) as well as clinically significant depressive symptoms during pregnancy (CES-D score&gt; 16, n = 46) compared with women without clinically significant symptoms (n = 327).</div></div><div><h3>Results</h3><div>CES-D scores were associated with differences in bacterial levels in the salivary microbiome. Women with clinically significant depressive symptoms (CES-D≥16) had significantly lower abundance in nine bacterial taxa, including the <em>Neisseria</em> genus, which has previously been positively associated with oral health and negatively correlated with pro-inflammatory cytokines, mental health, and infant birth weight. Findings were not explained by body mass index, smoking, antibiotic administration, oral health problems, or gestational week. Prediction tools based on 16S sequences indicated that significantly lower levels of several pathways related to the biosynthesis of Menaquinol, Ectoine biosynthesis, and D-glucarate degradation, were associated with women with depressive symptoms.</div></div><div><h3>Conclusions</h3><div>Our findings underscore the potential relationship between the oral microbiome and antenatal depression, highlighting microbiome measures as a promising source of biomarkers for maternal mental health. This study suggests previously unexplored aspects for understanding the microbiome's composition in women with mental health problems, emphasizing the need for further longitudinal investigations to elucidate the temporal dynamics of the oral microbiome in pregnancy.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"45 ","pages":"Article 100978"},"PeriodicalIF":3.7,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697249","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}