Brain, behavior, & immunity - health最新文献

{"title":"A review of neurophysiological relationships between sleep disorders and depression","authors":"Yifan Huang","doi":"10.1016/j.bbih.2026.101171","DOIUrl":"10.1016/j.bbih.2026.101171","url":null,"abstract":"<div><div>This review critically synthesizes current neurophysiological findings on the comorbidity between depression and sleep disorders. Drawing upon a multidisciplinary body of literature, the paper delineates overlapping neurochemical, hormonal, and inflammatory mechanisms. Further, it explores the role of astrocytic dysfunction and glutamate-GABA imbalance in reinforcing pathological feedback loops. By adopting an integrative framework, this review underscores the bidirectional and systemic nature of sleep disorder-depression comorbidity, offering insights into shared pathophysiological substrates and potential therapeutic targets for future research.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101171"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145980267","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":"Quantitative and morphological analyses reveal microglia-specific neuroinflammation in brain regions linked to cognitive function in ovariectomized and chronic intermittent hypoxia-exposed female rats","authors":"Cephas B. Appiah ,&nbsp;Kishor Kunwar ,&nbsp;Rebecca L. Cunningham ,&nbsp;J. Thomas Cunningham","doi":"10.1016/j.bbih.2026.101168","DOIUrl":"10.1016/j.bbih.2026.101168","url":null,"abstract":"<div><div>Women affected by obstructive sleep apnea (OSA) face an increased risk of cognitive impairment and mood disorders, with emerging evidence suggesting that neuroinflammation plays a significant role in the pathophysiology. OSA causes intermittent hypoxia and activates the immune response in the brain. Additionally, menopause is a separate risk factor that can put women with OSA at an even higher risk of cognitive decline. Although neuroinflammation occurs in OSA, the underlying mechanisms of the neuroinflammatory response are not well understood, and it remains unknown whether ovarian hormones modify these mechanisms. To examine the impact of OSA and hormone status on neuroinflammation, we used a 7-day chronic intermittent hypoxia (CIH) and ovariectomy (OVX) to model OSA and hormone status in female rats, respectively. To examine neuroinflammation, we investigated changes in brain microglia and astrocyte morphology and the number of reactive cells. We used a comprehensive three-dimensional reconstruction and analysis of microglia and astrocytes to study the changes in the morphology of these cells. We focused on brain regions associated with cognitive function (CA1 of the dorsal hippocampus, medial prefrontal cortex – mPFC, caudate and putamen – CP). Specifically, immunofluorescence of Iba1 (microglia marker) and GFAP (astrocyte marker) was conducted, along with measuring indicators of glial reactivity (branching, complexity, cell size, and number of reactive cells). Our results found that there were CIH and hormone effects on neuroinflammation in these brain regions. Microglia activation was impacted by an interaction between CIH and hormone status in all regions examined. In contrast, astrocytes showed no reactivity in all regions examined, regardless of CIH or hormone status. These findings suggest that menopause and OSA may impact microglia remodeling in brain areas associated with cognitive function. Microglia-specific neuroinflammation may be part of early mechanisms that lead to the cognitive impairments observed in CIH and hormone loss in females.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101168"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145979616","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":"A network analysis of lifetime stressor exposure, mental health, well-being, and immune cell mobilisation to acute stressors in young adults","authors":"Ella McLoughlin ,&nbsp;Daniele Magistro ,&nbsp;Roberto Vagnetti ,&nbsp;George M. Slavich ,&nbsp;James E. Turner ,&nbsp;Rachel Arnold ,&nbsp;Lee J. Moore ,&nbsp;John Hough","doi":"10.1016/j.bbih.2026.101186","DOIUrl":"10.1016/j.bbih.2026.101186","url":null,"abstract":"<div><div>Many young adults experience mental ill-health which is increasing over time. From a theoretical perspective, the accumulation of stressors experienced over the lifespan may be an important factor in influencing the mental health and well-being of young adults. Although continued exposure to stressors can negatively impact aspects of immunity, researchers have yet to examine how lifetime stressor exposure (i.e., frequency and severity) influences mental ill-health and well-being, and how these states subsequently affected immune cell mobilisation in response to a laboratory-based social stressor in young adults. Eighty-six participants (<em>M</em>_<em>age</em> = 23.31 years, <em>SD</em> = 4.94) completed an online questionnaire which assessed their exposure to lifetime stressors, symptoms of depression and anxiety, and levels of well-being. Next, participants completed the Trier Social Stress Test while immunological (i.e., lymphocytes, monocytes and neutrophils) data were collected immediately pre and post the test. Results revealed that the more frequent and severe stressors experienced during early life rendered individuals more susceptible to stressors during adulthood, which positively influenced symptoms of depression and subsequent anxiety. These aspects then deterred well-being, which negatively affected immune cell mobilisation to the acute stressor. The results highlight the potential importance of assessing lifetime stressor exposure for researchers and clinicians aiming to study the social-environmental drivers of poor immune and clinical health.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101186"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078576","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":"Stable serum peptidoglycan fragment levels do not support leaky gut in the acute phase or at one month following “mild” traumatic brain injury: A preliminary study","authors":"Koen Visser ,&nbsp;Yue Wang ,&nbsp;Jon D. Laman ,&nbsp;Myrthe E. de Koning ,&nbsp;Xiaoli Xu ,&nbsp;Andrei A. Vakhtin ,&nbsp;Andrew R. Mayer ,&nbsp;Daan Kremer ,&nbsp;Stephan J.L. Bakker ,&nbsp;Harry van Goor ,&nbsp;Joukje van der Naalt ,&nbsp;Arno R. Bourgonje ,&nbsp;Harm J. van der Horn","doi":"10.1016/j.bbih.2026.101192","DOIUrl":"10.1016/j.bbih.2026.101192","url":null,"abstract":"<div><div>The gut-brain axis is increasingly recognized as contributor to the pathophysiology of brain disorders, in part through its influence on inflammation. Impaired gut health can lead to so-called <em>leaky gut,</em> allowing bacterial cell wall fragments such as peptidoglycan-derived muramyl dipeptide (MDP) to translocate to the circulation. MDP can activate microglia, key mediators of neuroinflammation, via the intracellular receptor nucleotide-binding oligomerization domain-containing protein 2 (NOD2). Although neuroinflammation is a hallmark of “mild” traumatic brain injury (mTBI), the link between leaky gut and mTBI remains largely unexplored.</div><div>This preliminary prospective study investigated whether mTBI leads to increased MDP levels and NOD2 activation in the acute phase (N = 246; median 106 min post-injury) and at a ∼1-month follow-up visit (N = 140; median 32 days) in an emergency department cohort, relative to healthy controls (HC; N = 31, with N = 26 at ∼1-month). Serum MDP concentration was measured using an indirect competitive ELISA. Engagement of the pro-inflammatory nuclear factor (NF)-κB pathway was measured in NOD2-transfected cells. Additionally, blood interleukin (IL)-6 and IL-10 levels were quantified. Clinical outcome was measured at six months post-injury using the extended Glasgow Outcome Scale and a symptom questionnaire.</div><div>Linear mixed effects models showed that concentrations of MDP remained stable across visits in both mTBI and HC (<em>P</em> = 0.62), with no significant main effect of group (<em>P</em> = 0.16) or group × visit interaction (<em>P</em> = 0.25). In contrast, for engagement of NF-κB signaling in NOD2-expressing cells, a significant group × visit interaction (<em>P</em> = 0.004) was observed, with an elevation in mTBI relative to HC at ∼1-month post-injury (<em>P</em> = 0.01, Cohen's <em>d</em> = 0.48), but not in the acute phase (<em>P</em> = 0.22, <em>d</em> = 0.22). This elevation was associated with higher IL-6 (β = 0.16, <em>P</em> = 0.02) and IL-10 (β = 0.17, <em>P</em> = 0.006) levels in the acute phase. No associations with clinical outcome were observed.</div><div>In conclusion, our preliminary null findings for serum MDP do not directly support the emergence of leaky gut in either the acute phase or at ∼1-month following mTBI. However, transient increases in MDP occurring during the first month cannot be ruled out based on our findings. Increased engagement of the NF-κB pathway in NOD2-expressing cells likely reflects (damage-associated) mechanisms other than MDP. Assessment of NF-κB signaling may serve as a useful marker for studying chronic (neuro)inflammation following mTBI, complementing interleukin responses in the acute phase, an avenue warranting further investigation.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101192"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146189480","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":"Quinolinic acid as trigger/biomarker of dysosmia/dysgeusia in patients with acute coronavirus disease 2019: A retrospective case-control study","authors":"Jun Tsukiji ,&nbsp;Shiro Koizume ,&nbsp;Tomoko Takahashi ,&nbsp;Shuji Murakami ,&nbsp;Hiroyuki Takahashi ,&nbsp;Sachiyo Mitsunaga ,&nbsp;Sho Nakamura ,&nbsp;Hiroto Narimatsu ,&nbsp;Yohei Miyagi","doi":"10.1016/j.bbih.2026.101175","DOIUrl":"10.1016/j.bbih.2026.101175","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Impaired smell/taste sensation (dysosmia/dysgeusia) are common manifestations of coronavirus disease 2019 (COVID-19). Scattered peripheral chemoreceptors and directly innervating central nerves from the brain to the receptors are responsible systems for perception in the human body. The shared neurotransmitter serotonin (5-HT) and neuroimmune modulators of the kynurenine (Kyn) pathway (KP) are metabolites derived from tryptophan (Trp). The synthesis of KP metabolites is initiated by the rate-limiting enzymes indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can activate Trp metabolism. Therefore, we investigated whether serum metabolites of Trp and IDO/TDO activity could serve as biomarkers for assessing smell/taste impairment (dysosmia/dysgeusia) in patients during the acute phase of COVID-19.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We conducted a retrospective case-control study. Among patients admitted with acute COVID-19 to our hospital between September 13, 2021, and September 30, 2023, those whose chief complaints included dysosmia/dysgeusia at admission were identified. These symptoms were confirmed by the attending physician for COVID-19. Patients were stratified based on the presence or absence of dysosmia and/or dysgeusia.&lt;/div&gt;&lt;div&gt;In both patient groups, serum concentrations of Trp, 5-HT, Kyn, kynurenic acid (KYNA), and quinolinic acid (QUIN) were measured using enzyme-linked immunosorbent assay. IDO/TDO activity was expressed as Kyn–Trp ratio (KTR). The relationships between these biomarkers and dysosmia/dysgeusia, as well as other clinical parameters and outcomes, were evaluated.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Of 520 patients admitted with COVID-19, 95 met the inclusion and exclusion criteria. Among them, 26 patients with dysosmia/dysgeusia (group A) and 26 patients without these symptoms (group B) were analyzed. No significant intergroup difference was observed in the average timepoint at blood sampling after COVID-19 onset (post-day from onset: pdo) (4.69 ± 2.51 days in group A &lt;em&gt;vs&lt;/em&gt;. 3.62 ± 2.22 in group B). Group A showed significantly lower Trp levels [median 9.70 μg/mL (range 4.59–13.89) &lt;em&gt;vs&lt;/em&gt;. 10.40 (7.52–13.34), &lt;em&gt;p&lt;/em&gt; = 0.031], and higher KTR [61.34 (40.47–384.2) &lt;em&gt;vs&lt;/em&gt;. 53.52 (26.13–86.64), &lt;em&gt;p&lt;/em&gt; &lt; 0.037] and QUIN levels [574.39 nM (100.39–11909) &lt;em&gt;vs&lt;/em&gt;. 443.65 (83.09–998.3), &lt;em&gt;p&lt;/em&gt; &lt; 0.0169]. No significant differences were observed in 5-HT or KYNA levels between groups. Almost all cases of dysosmia involved anosmia/hyposmia and were significantly correlated with non-vaccination status with mRNA vaccine (&lt;em&gt;p&lt;/em&gt; = 0.017). In contrast, dysgeusia exhibited heterogeneous manifestations, primarily ageusia or hypogeusia, followed by hypersensitivity to salty taste, and was not correlated with vaccination status.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Clinically, serum K","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101175"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146038514","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":"Macrostructural, microstructural, and cellular effects of neuroinflammation on the mouse brain","authors":"Yash Patel ,&nbsp;Anita Woo ,&nbsp;Sammy Shun Wai Shi ,&nbsp;Eric Kim ,&nbsp;Jean Shin ,&nbsp;Yohan Yee ,&nbsp;Jason P. Lerch ,&nbsp;Brian J. Nieman ,&nbsp;Tomas Paus ,&nbsp;Zdenka Pausova","doi":"10.1016/j.bbih.2026.101178","DOIUrl":"10.1016/j.bbih.2026.101178","url":null,"abstract":"<div><div>Neuroinflammation is increasingly implicated in post-infectious brain atrophy and cognitive impairment, as well as the etiology of neurodegenerative and psychiatric disorders. Here, we employed an established mouse model of neuroinflammation (systemic lipopolysaccharide [LPS]) and studied its macrostructural, microstructural, and cellular effects on the mouse brain. We combined whole-brain two-photon microscopy, multiparametric magnetic resonance imaging, and <em>in silico</em> transcriptomics. We demonstrate that LPS increases microglial soma size, a marker of microglial proinflammatory transformation, throughout the brain. LPS also induces <em>in vivo</em> volumetric increases of multiple brain regions, but not of the cerebral cortex. These <em>in vivo</em> increases are no longer observed <em>ex vivo</em> (post-fixation), suggesting they may be due to brain edema. Moreover, LPS induces microstructural alterations, as indicated by <em>ex vivo</em> reductions in fractional anisotropy and magnetization transfer ratio, which were most pronounced in the cerebral cortex. These reductions had the largest effect size in regions with higher expression of genes specific to parvalbumin inhibitory neurons and excitatory layer 4/5 intratelencephalic neurons, which were enriched in genes encoding synapse components. Thus, these results suggest that LPS-induced neuroinflammation may lead to brain edema, which spares the cerebral cortex, and microstructural alterations, which impact the cerebral cortex and may involve specific subtypes of inhibitory and excitatory neurons and their synapses.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101178"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078573","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":"Early-life maternal probiotic supplementation programs sex- and region–specific gene expression in the adult offspring brain","authors":"Tatiana Siegler Lathrop ,&nbsp;Inés Martínez Sanchez ,&nbsp;Ioannis S. Chronakis ,&nbsp;Rochellys Diaz Heijtz","doi":"10.1016/j.bbih.2026.101191","DOIUrl":"10.1016/j.bbih.2026.101191","url":null,"abstract":"<div><h3>Background</h3><div>The maternal perinatal environment shapes brain development and long-term neurodevelopmental trajectories. Probiotic supplementation during this period has emerged as a promising strategy to support healthy neurodevelopmental outcomes through modulation of immune and synaptic plasticity pathways. However, the persistence and specificity of molecular effects in the offspring brain, particularly with respect to sex and brain region, remain poorly understood.</div></div><div><h3>Methods</h3><div>We conducted two independent mouse experiments using different probiotic strains and exposure windows to evaluate the long-term transcriptional effects of maternal probiotic supplementation. Time-mated C57BL/6JRj dams received a multi-species probiotic (Ecologic® Panda) from gestational day (GD) 6 until birth, whereas BALB/cJRj dams received <em>Limosilactobacillus reuteri</em> (<em>L. reuteri</em>) from GD6 through postnatal day 7. The hippocampus and hypothalamus from adult male and female offspring were analyzed by RT-qPCR for genes related to synaptic plasticity, oxytocin signaling, neuroimmune regulation, myelination, and peptidoglycan (PGN) transport.</div></div><div><h3>Results</h3><div>Multi-species supplementation induced broad and persistent transcriptional changes in hippocampus and hypothalamus, with generally larger effects in males. Altered transcripts included markers of synaptic plasticity (<em>Bdnf</em>, <em>Ppp1r1b</em>, <em>Syp</em>), immune regulation (<em>Il10, Trem2</em>), myelination (<em>Mag</em>, <em>Mog</em>), oxytocin signaling (<em>Oxtr</em>), and PGN transport (<em>Slc15a1</em>, <em>Slc15a2</em>, <em>Slc46a2</em>). In contrast, <em>L. reuteri</em> produced selective, sex- and region-dependent transcriptional effects that differed by brain region and sex. Notably, across probiotic conditions, <em>Il10</em> was consistently upregulated in both brain regions and sexes.</div></div><div><h3>Conclusions</h3><div>These findings highlight that short, targeted maternal probiotic supplementation during the perinatal period is associated with persistent molecular signatures in the adult offspring brain across genetic backgrounds, converging on neuroimmune-related pathways.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101191"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146189482","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":"Assessing the repurposing potential of disease-modifying antirheumatic drug targets to reduce Alzheimer's disease risk: a Mendelian randomization study","authors":"Christina N. Kushnir ,&nbsp;Victoria Taylor-Bateman ,&nbsp;Neil M. Davies ,&nbsp;Emma L. Anderson","doi":"10.1016/j.bbih.2026.101185","DOIUrl":"10.1016/j.bbih.2026.101185","url":null,"abstract":"<div><h3>Background</h3><div>Systemic inflammation plays a key role in the development and progression of Alzheimer's disease (AD). However, the repurposing potential of select anti-inflammatory drug targets for AD treatment remains unclear.</div></div><div><h3>Methods</h3><div>Two-sample Mendelian randomization (MR) and colocalization analyses were conducted to estimate the effects of select disease-modifying antirheumatic (DMARD) targets on AD risk. We investigated 9 DMARD targets, using blood protein quantitative trait loci (pQTLs) from the UK Biobank Pharma Proteomics Project (<em>n</em> = 54,219). Outcome associations were extracted from the International Genomics of Alzheimer's Project (<em>n</em>cases = 21,982, <em>n</em>controls = 41,944).</div></div><div><h3>Results</h3><div>Our MR estimates suggest that higher levels of <em>FCGR3B</em>, an etanercept target, increased the risk of AD (OR: 1.10; 95% CI [1.02, 1.19]; <em>p</em> = 0.01). We found little evidence that the remaining DMARD targets affected AD risk. Colocalization analysis provided little evidence that target pQTLs, including <em>FCGR3B</em>, colocalized with AD.</div></div><div><h3>Conclusions</h3><div>Our findings suggest a causal effect of <em>FCGR3B</em> on AD risk, but not for the remainder of the analyzed DMARD targets. Further research is recommended to elucidate the causal role of <em>FCGR3B</em> in AD and build upon the current literature on viable AD therapeutic targets.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101185"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146189476","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":"AQP4-IgG and mood disorders: Case series of neuromyelitis optica spectrum disorder","authors":"Qing Xu ,&nbsp;Yanlin Han ,&nbsp;Shuzhan Gao ,&nbsp;Siyi Wang ,&nbsp;Yanyan Lu ,&nbsp;Kuan-Pin Su ,&nbsp;Xijia Xu","doi":"10.1016/j.bbih.2026.101177","DOIUrl":"10.1016/j.bbih.2026.101177","url":null,"abstract":"<div><div>Neuromyelitis optica spectrum disorders (NMOSD) are autoimmune inflammatory demyelinating conditions primarily affecting the optic nerves and spinal cord. While NMOSD pathogenesis is mediated by aquaporin-4 antibody (AQP4-IgG) autoimmunity, increasing evidence suggests significant comorbidity with affective symptoms. The neuropathological mechanisms underlying this comorbidity, however, remain incompletely understood. We reported two cases of female patients with concurrent NMOSD and mood disorders that illustrate a shared neuroinflammatory etiology. Case 1, a 26-year-old female, presented with a decade-long history of mood instability, diagnosed as bipolar disorder (BD) mixed episode, which coincided with her NMOSD diagnosis. Case 2, a 25-year-old female, initially presented with major depressive disorder (MDD) but was subsequently diagnosed with NMOSD following the acute onset of neurological symptoms. Both patients were, serum AQP4-IgG positive and exhibited demyelinating changes in the frontal lobe. Following immunosuppressive and psychiatric treatment, both patients experienced marked improvement in neurological function, suicidality, and affective symptoms. These case reports suggest a bidirectional relationship between NMOSD and mood disorders, likely mediated by AQP4-IgG-driven neuroinflammatory responses. AQP4-IgG screening may serve as a critical tool to distinguish organic mood disorder from primary psychiatric conditions, particularly in patients with atypical neurological symptoms.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101177"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145980266","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 emerging role of lymphocytes in post-stroke inflammation: A treatable target and review of current pharmacological evidence in humans\"","authors":"A. Papageorgiou ,&nbsp;D. Chatzistefanidis ,&nbsp;M. Nikolakea ,&nbsp;N.-R. Karela ,&nbsp;M. Gkrampovari ,&nbsp;K. Lantavos ,&nbsp;D. Bartzi ,&nbsp;L. Traikov ,&nbsp;S. Markoula","doi":"10.1016/j.bbih.2026.101172","DOIUrl":"10.1016/j.bbih.2026.101172","url":null,"abstract":"<div><div>Acute ischemic stroke is one of the leading causes of mortality and morbidity worldwide. The underlying inflammation process following the ischemic event arises as an important factor of great therapeutic interest. Recent research has showcased the roles of B- and T-lymphocytes in the acute post-stroke period, with various types of lymphocytes affecting differently the clinical outcome of the patient. Herein, we reviewed the literature and discussed the functional role of various subpopulations of lymphocytes in recovery and repair of the ischemic tissue as well as their influence on the final outcome of the patient. Additionally, we searched the literature regarding current knowledge on various drugs possibly affecting neuroinflammation or exhibiting a neuroprotective role in the acute post-stroke period.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101172"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146038516","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}