Brain, behavior, & immunity - health最新文献

{"title":"In a circuit necessary for cognition and emotional affect, Alzheimer's-like pathology associates with neuroinflammation, cognitive and motivational deficits in the young adult TgF344-AD rat","authors":"Caesar M. Hernandez ,&nbsp;Macy A. McCuiston ,&nbsp;Kristian Davis ,&nbsp;Yolanda Halls ,&nbsp;Juan Pablo Carcamo Dal Zotto ,&nbsp;Nateka L. Jackson ,&nbsp;Lynn E. Dobrunz ,&nbsp;Peter H. King ,&nbsp;Lori L. McMahon","doi":"10.1016/j.bbih.2024.100798","DOIUrl":"10.1016/j.bbih.2024.100798","url":null,"abstract":"<div><p>In addition to extracellular amyloid plaques, intracellular neurofibrillary tau tangles, and inflammation, cognitive and emotional affect perturbations are characteristic of Alzheimer's disease (AD). The cognitive and emotional domains impaired by AD include several forms of decision making (such as intertemporal choice), blunted motivation (increased apathy), and impaired executive function (such as working memory and cognitive flexibility). However, the interaction between these domains of the mind and their supporting neurobiological substrates at prodromal stages of AD, or whether these interactions can be predictive of AD severity (individual variability), remain unclear. In this study, we employed a battery of cognitive and emotional tests in the young adult (5–7 mo) transgenic Fisher-344 AD (TgF344-AD; TgAD) rat model of AD. We also assessed whether markers of inflammation or AD-like pathology in the prelimbic cortex (PrL) of the medial prefrontal cortex (mPFC), basolateral amygdala (<span>BLA</span>), or nucleus accumbens (NAc), all structures that directly support the aforementioned behaviors, were predictive of behavioral deficits. We found TgAD rats displayed maladaptive decision making, greater apathy, and impaired working memory that was indeed predicted by AD-like pathology in the relevant brain structures, even at an early age. Moreover, we report that the BLA is an early epicenter of inflammation, and notably, AD-like pathology in the PrL, BLA, and NAc was predictive of BLA inflammation. These results suggest that operant-based battery testing may be sensitive enough to determine pathology trajectories, including neuroinflammation, from early stages of AD.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"39 ","pages":"Article 100798"},"PeriodicalIF":3.7,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000760/pdfft?md5=0989e8198e3c0f2ac742ef847040c6e8&pid=1-s2.0-S2666354624000760-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141394741","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":"Recurrent COVID-19-related psychotic disorder with neuro-immuno-endocrine dysfunction as a possible underlying mechanism: A case report from China","authors":"Chenghui Yang ,&nbsp;Ying He ,&nbsp;Lu Yuan ,&nbsp;Cui Yuan ,&nbsp;Fan Chang ,&nbsp;Wenqian Feng ,&nbsp;Bo Zhou","doi":"10.1016/j.bbih.2024.100803","DOIUrl":"10.1016/j.bbih.2024.100803","url":null,"abstract":"<div><h3>Background</h3><p>SARS-CoV-2, first identified in Wuhan, China, in December 2019, has been gradually spreading worldwide since 2020. The relationship between SARS-CoV-2 infection and psychotic disorders has received much attention, and several studies have described the direct/indirect mechanisms of its effects on the brain, but no mechanism has been found to explain recurrent episodes of COVID-19-related psychotic symptoms.</p></div><div><h3>Case</h3><p>We report the case of an 18-year-old female patient with no family or personal psychotic disorder history with multiple hospital admissions with symptoms such as disorganized speech and behavior, hyperactivity, restlessness, and impulsive aggression during the COVID-19 recovery period. Relevant tests revealed longitudinal changes such as persistent IL-6 and IL-10 elevation, abnormal discharges on EEG, and brain and hippocampal MRI abnormal signals. The patient was treated with antipsychotics, MECT, combination therapy of hormones and antivirals, then discharged after multiple treatment rounds.</p></div><div><h3>Conclusion</h3><p>The case presented here outlines the possibility that the COVID-19 recovery period may be a critical period for acute psychotic episodes and that the patient's recurrent psychotic symptoms may be associated with neuro-immuno-endocrine dysfunction mediated by sustained cytokine synthesis, further causing structural and functional brain damage. Routine psychiatric evaluation and related screening should be performed at all stages of the illness to better identify, prevent, and effectively intervene in psychiatric disorders following COVID-19. Because many outcomes require long-term assessment, a clearer understanding of the impact of the COVID-19 epidemic on mental health is likely to emerge in the future.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"39 ","pages":"Article 100803"},"PeriodicalIF":3.7,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000814/pdfft?md5=38c5c8fdbfd7d4763c09aa5111b40c99&pid=1-s2.0-S2666354624000814-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141402265","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":"Anti-spike antibody responses to SARS-CoV-2 mRNA vaccines in people with schizophrenia and schizoaffective disorder","authors":"Katlyn Nemani ,&nbsp;Livia De Picker ,&nbsp;Faith Dickerson ,&nbsp;Marion Leboyer ,&nbsp;Michele Santacatterina ,&nbsp;Fumika Ando ,&nbsp;Gillian Capichioni ,&nbsp;Thomas E. Smith ,&nbsp;Jamie Kammer ,&nbsp;Kawtar El Abdellati ,&nbsp;Manuel Morrens ,&nbsp;Violette Coppens ,&nbsp;Emily Katsafanas ,&nbsp;Andrea Origoni ,&nbsp;Sabahat Khan ,&nbsp;Kelly Rowe ,&nbsp;R.Sarah Ziemann ,&nbsp;Ryad Tamouza ,&nbsp;Robert H. Yolken ,&nbsp;Donald C. Goff","doi":"10.1016/j.bbih.2024.100802","DOIUrl":"10.1016/j.bbih.2024.100802","url":null,"abstract":"<div><h3>Importance</h3><p>Individuals with schizophrenia are at higher risk for severe COVID-19 illness and severe breakthrough infection following vaccination. It is unclear whether immune response to vaccination differs in this population.</p></div><div><h3>Objective</h3><p>To assess whether anti-SARS-CoV-2 spike antibody titers after vaccination differ in people with a diagnosis of schizophrenia or schizoaffective disorder (SZ) compared to controls without a psychiatric disorder.</p></div><div><h3>Design</h3><p>This cohort study assessed antibody response following the first and second dose of mRNA vaccines at longitudinal timepoints, up to 7 weeks following the first dose of vaccine.</p></div><div><h3>Setting</h3><p>A multi-center study including psychiatric healthcare settings in the United States and Europe.</p></div><div><h3>Participants</h3><p>205 adults with no history of COVID-19 infection, including 106 individuals with SZ and 99 controls without a psychiatric disorder, who received their first dose of SARS-CoV-2 mRNA vaccine between December 20, 2020 and May 27, 2021.</p></div><div><h3>Main outcomes and measures</h3><p>Mean SARS-CoV-2 anti-Spike IgG antibody levels within 7 weeks after the first dose of vaccination.</p></div><div><h3>Results</h3><p>A total of 205 individuals (mean [SD] age, 44.7 [12.0] years; 90 [43.9%] male) were included, of which 106 (51.7%) were diagnosed with SZ. SZ was associated with lower mean log antibody levels (−0.15; 95% CI, −0.27 to −0.03, <em>P</em> = 0.016) after adjusting for age, sex, body mass index, smoking, days since vaccination, and vaccine manufacturer. In secondary analyses of dose-specific responses, SZ was associated with a lower mean log antibody level after the second dose of vaccine (−0.23; 95% CI -0.39 to −0.06, <em>P</em> = 0.006), but not the first dose of vaccine (0.00; 95% CI -0.18— 0.19, <em>P</em> = 0.96).</p></div><div><h3>Conclusions and Relevance</h3><p>In this cohort study of individuals with SZ and a control group without psychiatric disorders, SZ was associated with lower SARS-CoV-2 anti-spike antibody levels following 2 doses of SARS-CoV-2 mRNA vaccination. This highlights the need for further studies assessing vaccine immunogenicity in individuals with schizophrenia.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100802"},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000802/pdfft?md5=be6f3f21a353c1ddec433f95d38a7fea&pid=1-s2.0-S2666354624000802-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141274974","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":"Prenatal and childhood air pollution exposure, cellular immune biomarkers, and brain connectivity in early adolescents","authors":"Devyn L. Cotter ,&nbsp;Jessica Morrel ,&nbsp;Kirthana Sukumaran ,&nbsp;Carlos Cardenas-Iniguez ,&nbsp;Joel Schwartz ,&nbsp;Megan M. Herting","doi":"10.1016/j.bbih.2024.100799","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100799","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;p&gt;Ambient air pollution is a neurotoxicant with hypothesized immune-related mechanisms. Adolescent brain structural and functional connectivity may be especially vulnerable to ambient pollution due to the refinement of large-scale brain networks during this period, which vary by sex and have important implications for cognitive, behavioral, and emotional functioning. In the current study we explored associations between air pollutants, immune markers, and structural and functional connectivity in early adolescence by leveraging cross-sectional sex-stratified data from the Adolescent Brain Cognitive Development℠ Study®.&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;p&gt;Pollutant concentrations of fine particulate matter, nitrogen dioxide, and ozone were assigned to each child's primary residential address during the prenatal period and childhood (9-10 years-old) using an ensemble-based modeling approach. Data collected at 11-13 years-old included resting-state functional connectivity of the default mode, frontoparietal, and salience networks and limbic regions of interest, intracellular directional and isotropic diffusion of available white matter tracts, and markers of cellular immune activation. Using partial least squares correlation, a multivariate data-driven method that identifies important variables within latent dimensions, we investigated associations between 1) pollutants and structural and functional connectivity, 2) pollutants and immune markers, and 3) immune markers and structural and functional connectivity, in each sex separately.&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;p&gt;Air pollution exposure was related to white matter intracellular directional and isotropic diffusion at ages 11–13 years, but the direction of associations varied by sex. There were no associations between pollutants and resting-state functional connectivity at ages 11–13 years. Childhood exposure to nitrogen dioxide was negatively correlated with white blood cell count in males. Immune biomarkers were positively correlated with white matter intracellular directional diffusion in females and both white matter intracellular directional and isotropic diffusion in males. Lastly, there was a reliable negative correlation between lymphocyte-to-monocyte ratio and default mode network resting-state functional connectivity in females, as well as a compromised immune marker profile associated with lower resting-state functional connectivity between the salience network and the left hippocampus in males. In post-hoc exploratory analyses, we found that the PLSC-identified white matter tracts and resting-state networks related to processing speed and cognitive control performance from the NIH Toolbox.&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;p&gt;We identified novel links between childhood nitrogen dioxide and cellular immune activation in males, and brain network connectivity and immune markers in both sexes. Future research should explore the potentially mediating role of immune ac","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100799"},"PeriodicalIF":0.0,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000772/pdfft?md5=031d4fbbb64aa71f9f659cff2014ec5c&pid=1-s2.0-S2666354624000772-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141313914","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 microbiota in autistic children: Diagnosis-related differences and associations with clinical characteristics","authors":"Margaux Evenepoel ,&nbsp;Nicky Daniels ,&nbsp;Matthijs Moerkerke ,&nbsp;Michiel Van de Vliet ,&nbsp;Jellina Prinsen ,&nbsp;Elise Tuerlinckx ,&nbsp;Jean Steyaert ,&nbsp;Bart Boets ,&nbsp;Kaat Alaerts ,&nbsp;Marie Joossens","doi":"10.1016/j.bbih.2024.100801","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100801","url":null,"abstract":"<div><p>Similar to the gut microbiome, oral microbiome compositions have been suggested to play an important role in the etiology of autism. However, empirical research on how variations in the oral microbiome relate to clinical-behavioral difficulties associated with autism remains sparse. Furthermore, it is largely unknown how potentially confounding lifestyle variables, such as oral health and nutrition, may impact these associations. To fill this gap, the current study examined diagnosis-related differences in oral microbiome composition between 80 school-aged autistic children (8–12 years; 64 boys, 16 girls) versus 40 age-matched typically developing peers (32 boys, 8 girls). In addition, associations with individual differences in social functioning (SRS-2), repetitive behavior (RBS-R) and anxiety (SCARED) were explored, as well as the impact of several lifestyle variables regarding nutrition and oral health. Results provide important indications that the bacterial genera <em>Solobacterium</em>, <em>Stomatobaculum</em>, <em>Ruminococcaceae UCG.014, Tannerella</em> and <em>Campylobacter</em> were significantly more abundant in autistic compared to non-autistic children. Furthermore, the former four bacteria that were significantly more abundant in the autistic children showed significant associations with parent-reported social difficulties, repetitive and restrictive behavior and with parent-reported anxiety-like behavior. Importantly, associations among oral microbiome and quantitative diagnostic characteristics were not significantly driven by differences in lifestyle variables. This exploratory study reveals significant differences in oral microbiome composition between autistic and non-autistic children, even while controlling for potential confounding lifestyle variables. Furthermore, the significant associations with clinical characteristics suggest that individual differences in microbiome composition might be involved in shaping the clinical phenotype of autism. However, these associations warrant further exploration of the oral microbiome's potential beyond the oral cavity and specifically with respect to neuropsychiatric conditions.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100801"},"PeriodicalIF":0.0,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000796/pdfft?md5=023a32b44592ac01c4a80c9277a345df&pid=1-s2.0-S2666354624000796-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141243522","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":"Risk factors associated with nocebo effects: A review of reviews","authors":"Francesca Grosso ,&nbsp;Diletta Barbiani ,&nbsp;Cesare Cavalera ,&nbsp;Eleonora Volpato ,&nbsp;Francesco Pagnini","doi":"10.1016/j.bbih.2024.100800","DOIUrl":"10.1016/j.bbih.2024.100800","url":null,"abstract":"<div><h3>Objective</h3><p>This meta-review aims to identify and categorize the risk factors that are associated with nocebo effects. The nocebo effect can exert a negative impact on treatment outcomes and have detrimental outcomes on health. Learning more about its potential predictors and risk factors is a crucial step to mitigating it.</p></div><div><h3>Methods</h3><p>Literature review studies about the risk factors for nocebo effects were searched through five databases (PubMed, Scopus, The Cochrane Library, PsycINFO, and Embase) and through grey literature. Methodological validity and risk of bias were assessed. We conducted a thematic analysis of the results of the forty-three included reviews.</p></div><div><h3>Results</h3><p>We identified nine categories of risk factors: prior expectations and learning; socio-demographic characteristics; personality and individual differences; neurodegenerative conditions; inflammatory conditions; communication of information and patient-physician relationship; drug characteristics; setting; and self-awareness. We also highlighted the main biochemical and neurophysiological mechanisms underlying nocebo effects.</p></div><div><h3>Conclusions</h3><p>Nocebo effects arise from expectations of adverse symptoms, particularly when triggered by previous negative experiences. A trusting relationship with the treating physician and clear, tailored treatment instructions can act as protective factors against a nocebo effect. Clinical implications are discussed.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100800"},"PeriodicalIF":0.0,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000784/pdfft?md5=cfbe3f05d2c6728a4a2f91afcd67d8f0&pid=1-s2.0-S2666354624000784-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141136327","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":"Disentangling factors contributing to individual differences and health disparities in chronic pain and whole person health with measures of allostatic load","authors":"Angela M. Mickle ,&nbsp;Jared J. Tanner ,&nbsp;Lisa H. Antoine ,&nbsp;Cynthia Garvan ,&nbsp;Song Lai ,&nbsp;Rene Przkora ,&nbsp;Jeffrey C. Edberg ,&nbsp;Roland Staud ,&nbsp;David Redden ,&nbsp;Burel R. Goodin ,&nbsp;Catherine C. Price ,&nbsp;Roger B. Fillingim ,&nbsp;Kimberly T. Sibille","doi":"10.1016/j.bbih.2024.100794","DOIUrl":"10.1016/j.bbih.2024.100794","url":null,"abstract":"","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100794"},"PeriodicalIF":0.0,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000723/pdfft?md5=8b4b9563a918c1832c3762e978319501&pid=1-s2.0-S2666354624000723-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141036243","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 potential role of the p75 receptor in schizophrenia: neuroimmunomodulation and making life or death decisions","authors":"Jessica Chandra","doi":"10.1016/j.bbih.2024.100796","DOIUrl":"10.1016/j.bbih.2024.100796","url":null,"abstract":"<div><p>The nerve growth factor receptor, also referred to as tumour necrosis factor II and the p75 neurotrophin receptor (p75), serves pleiotropic functions in both the peripheral and central nervous system, involving modulation of immune responses, cell survival and cell death signalling in response to multiple ligands including cytokines such as TNFα, as well as proneurotrophins and mature neurotrophins. Whilst <em>in vitro</em> and <em>in vivo</em> studies have characterised various responses of the p75 receptor in isolated conditions, it remains unclear whether the p75 receptor serves to provide neuroprotection or contributes to neurotoxicity in neuroinflammatory and neurotrophin-deficit conditions, such as those presenting in schizophrenia. The purpose of this mini-review is to characterise the potential signalling mechanisms of the p75 receptor respective to neuropathological changes prevailing in schizophrenia to ultimately propose how specific functions of the receptor may underlie altered levels of p75 in specific cell types. On the basis of this evaluation, this mini-review aims to promote avenues for future research in utilising the therapeutic potential of ligands for the p75 receptor in psychiatric disorders, whereby heightened inflammation and reductions in trophic signalling mechanisms coalesce in the brain, potentially resulting in tissue damage.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100796"},"PeriodicalIF":0.0,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000747/pdfft?md5=9361680cdab4a5b2d9b7ecfe64cdb29f&pid=1-s2.0-S2666354624000747-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141046503","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":"Trait-anxiety and glial-related neuroinflammation of the amygdala and its associated regions in Alzheimer's disease: A significant correlation","authors":"Fumihiko Yasuno ,&nbsp;Yasuyuki Kimura ,&nbsp;Aya Ogata ,&nbsp;Hiroshi Ikenuma ,&nbsp;Junichiro Abe ,&nbsp;Hiroyuki Minami ,&nbsp;Takashi Nihashi ,&nbsp;Kastunori Yokoi ,&nbsp;Saori Hattori ,&nbsp;Nobuyoshi Shimoda ,&nbsp;Atsushi Watanabe ,&nbsp;Kensaku Kasuga ,&nbsp;Takeshi Ikeuchi ,&nbsp;Akinori Takeda ,&nbsp;Takashi Sakurai ,&nbsp;Kengo Ito ,&nbsp;Takashi Kato","doi":"10.1016/j.bbih.2024.100795","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100795","url":null,"abstract":"<div><h3>Background</h3><p>Positron emission tomography, which assesses the binding of translocator protein radiotracers, ¹¹C-DPA-713, may be a sensitive method for determining glial-mediated neuroinflammation levels. This study investigated the relationship between regional ¹¹C-DPA713 binding potential (BP_ND) and anxiety in patients with Alzheimer's disease (AD) continuum.</p></div><div><h3>Methods</h3><p>Nineteen patients with AD continuum determined to be amyloid-/p-tau 181-positive via cerebrospinal fluid analysis were included in this cross-sectional study (mild cognitive impairment [MCI, n = 5] and AD [n = 14]). Anxiety was evaluated using the State-Trait Anxiety Inventory (STAI). A whole-brain voxel-based analysis was performed to examine the relationship between ¹¹C-DPA-713-BP_ND values at each voxel and the STAI score. Stepwise multiple regression analysis was performed to determine the predictors of STAI scores using independent variables, including ¹¹C-DPA-713-BP_ND values within significant clusters. ¹¹C-DPA-713-BP_ND values were compared between patients with AD continuum with low-to-moderate and high STAI scores.</p></div><div><h3>Results</h3><p>Voxel-based analysis revealed a positive correlation between trait anxiety severity and ¹¹C-DPA713-BP_ND values in the centromedial amygdala and the left inferior occipital area [<em>P</em> &lt; 0.001 (uncorrected) at the voxel-level]. ¹¹C-DPA713-BP_ND values in these regions were a strong predictor of the STAI trait anxiety score. Specifically, patients with AD continuum and high trait anxiety had increased ¹¹C-DPA713-BP_ND values in these regions.</p></div><div><h3>Conclusions</h3><p>The amygdala–occipital lobe circuit influences the control of emotional generation, and disruption of this network by AD pathology-induced inflammation may contribute to the expression of anxiety. Our findings suggest that suppression of inflammation can help effectively treat anxiety by attenuating damage to the amygdala and its associated areas.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100795"},"PeriodicalIF":0.0,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000735/pdfft?md5=aef1dfda9e83d8bff04169208c9888b1&pid=1-s2.0-S2666354624000735-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140948809","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":"Sleep fragmentation after traumatic brain injury impairs behavior and conveys long-lasting impacts on neuroinflammation","authors":"Samuel Houle ,&nbsp;Zoe Tapp ,&nbsp;Shannon Dobres ,&nbsp;Sakeef Ahsan ,&nbsp;Yvanna Reyes ,&nbsp;Christopher Cotter ,&nbsp;Jessica Mitsch ,&nbsp;Zachary Zimomra ,&nbsp;Juan Peng ,&nbsp;Rachel K. Rowe ,&nbsp;Jonathan Lifshitz ,&nbsp;John Sheridan ,&nbsp;Jonathan Godbout ,&nbsp;Olga N. Kokiko-Cochran","doi":"10.1016/j.bbih.2024.100797","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100797","url":null,"abstract":"<div><p>Traumatic brain injury (TBI) causes a prolonged inflammatory response in the central nervous system (CNS) driven by microglia. Microglial reactivity is exacerbated by stress, which often provokes sleep disturbances. We have previously shown that sleep fragmentation (SF) stress after experimental TBI increases microglial reactivity and impairs hippocampal function 30 days post-injury (DPI). The neuroimmune response is highly dynamic the first few weeks after TBI, which is also when injury induced sleep-wake deficits are detected. Therefore, we hypothesized that even a few weeks of TBI SF stress would synergize with injury induced sleep-wake deficits to promote neuroinflammation and impair outcome. Here, we investigated the effects of environmental SF in a lateral fluid percussion model of mouse TBI. Half of the mice were undisturbed, and half were exposed to 5 h of SF around the onset of the light cycle, daily, for 14 days. All mice were then undisturbed 15–30 DPI, providing a period for SF stress recovery (SF-R). Mice exposed to SF stress slept more than those in control housing 7–14 DPI and engaged in more total daily sleep bouts during the dark period. However, SF stress did not exacerbate post-TBI sleep deficits. Testing in the Morris water maze revealed sex dependent differences in spatial reference memory 9–14 DPI with males performing worse than females. Post-TBI SF stress suppressed neurogenesis-related gene expression and increased inflammatory signaling in the cortex at 14 DPI. No differences in sleep behavior were detected between groups during the SF stress recovery period 15–30 DPI. Microscopy revealed cortical and hippocampal IBA1 and CD68 percent-area increased in TBI SF-R mice 30 DPI. Additionally, neuroinflammatory gene expression was increased, and synaptogenesis-related gene expression was suppressed in TBI-SF mice 30 DPI. Finally, IPA canonical pathway analysis showed post-TBI SF impaired and delayed activation of synapse-related pathways between 14 and 30 DPI. These data show that transient SF stress after TBI impairs recovery and conveys long-lasting impacts on neuroimmune function independent of continuous sleep deficits. Together, these finding support that even limited exposure to post-TBI SF stress can have lasting impacts on cognitive recovery and regulation of the immune response to trauma.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"38 ","pages":"Article 100797"},"PeriodicalIF":0.0,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000759/pdfft?md5=6ebb683a4c8c8c43bd3ddd98240f5f67&pid=1-s2.0-S2666354624000759-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140950748","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}