Biological psychiatry global open science最新文献

{"title":"Guide for Authors","authors":"","doi":"10.1016/S2667-1743(24)00064-8","DOIUrl":"10.1016/S2667-1743(24)00064-8","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100351"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000648/pdfft?md5=8e33f4496acd15507ecfb2b321bacf5e&pid=1-s2.0-S2667174324000648-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623574","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":"Editorial Board Page","authors":"","doi":"10.1016/S2667-1743(24)00061-2","DOIUrl":"10.1016/S2667-1743(24)00061-2","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100348"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000612/pdfft?md5=4f6f0078669bf5335ccc8a2e1a3d4c61&pid=1-s2.0-S2667174324000612-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623571","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":"Targeting the Hippocampus in the Context of Trauma","authors":"Sanne J.H. van Rooij","doi":"10.1016/j.bpsgos.2024.100335","DOIUrl":"10.1016/j.bpsgos.2024.100335","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100335"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266717432400048X/pdfft?md5=5ad797f21fe297e1ba10d663f2c2993a&pid=1-s2.0-S266717432400048X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623581","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":"Misperceiving Momentum: Computational Mechanisms of Biased Striatal Reward Prediction Errors in Bipolar Disorder","authors":"Hestia Moningka ,&nbsp;Liam Mason","doi":"10.1016/j.bpsgos.2024.100330","DOIUrl":"10.1016/j.bpsgos.2024.100330","url":null,"abstract":"<div><h3>Background</h3><p>Dysregulated reward processing and mood instability are core features of bipolar disorder that have largely been considered separately, with contradictory findings. We sought to test a mechanistic account that emphasizes an excessive tendency in bipolar disorder to enter recursive cycles in which reward perception is biased by signals that the environment may be changing for the better or worse.</p></div><div><h3>Methods</h3><p>Participants completed a probabilistic reward task with functional magnetic resonance imaging. Using an influential computational model, we ascertained whether participants with bipolar disorder (<em>n</em> = 21) showed greater striatal tracking of momentum-biased reward prediction errors (RPEs) than matched control participants (<em>n</em> = 21). We conducted psychophysiological interaction analyses to quantify the degree to which each group modulated functional connectivity between the ventral striatum and left anterior insula in response to fluctuations in momentum.</p></div><div><h3>Results</h3><p>In participants with bipolar disorder, but not control participants, the momentum-biased RPE model accounted for significant additional variance in striatal activity beyond a standard model of veridical RPEs. Compared with control participants, participants with bipolar disorder exhibited lower insular-striatal functional connectivity modulated by momentum-biased RPEs, an effect that was more pronounced as a function of current manic symptoms.</p></div><div><h3>Conclusions</h3><p>Consistent with existing theory, we found evidence that bipolar disorder is associated with a tendency for momentum to excessively bias striatal tracking of RPEs. We identified impaired insular-striatal connectivity as a possible locus for this propensity. We argue that computational psychiatric approaches that examine momentary shifts in reward and mood dynamics have strong potential for yielding new mechanistic insights and intervention targets.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100330"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000430/pdfft?md5=fec0e6195a7b2242719484cff2576524&pid=1-s2.0-S2667174324000430-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623582","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":"Distinct Mindfulness States Produce Dissociable Effects on Neural Markers of Emotion Processing: Evidence From the Late Positive Potential","authors":"Yanli Lin ,&nbsp;Marne L. White ,&nbsp;Deanna Wu ,&nbsp;Natee Viravan ,&nbsp;Todd S. Braver","doi":"10.1016/j.bpsgos.2024.100357","DOIUrl":"10.1016/j.bpsgos.2024.100357","url":null,"abstract":"<div><h3>Background</h3><p>Mindfulness has long been theorized to benefit emotion regulation, but despite the ubiquity of the claim, there is little empirical evidence demonstrating how mindfulness modulates the neurophysiology of emotion processing. The current study aimed to fill this gap in knowledge by leveraging a novel research approach capable of discretizing mindfulness into distinct states of open monitoring (OM) and focused attention (FA) to distinguish their influence on multimodal subjective and objective measures of emotion processing.</p></div><div><h3>Methods</h3><p>Utilizing a fully within-participant picture viewing state induction protocol (<em>N</em> = 30), we compared the effects of OM and FA, rigorously contrasted against an active control, on the visually evoked late positive potential (LPP), a neural index of motivated attention. Bayesian mixed modeling was used to distinguish OM versus FA effects on the early and late sustained LPP while evaluating the influence of subjective arousal ratings as a within-participant moderator of the state inductions.</p></div><div><h3>Results</h3><p>When negative picture trials were retrospectively rated as more subjectively arousing, the OM induction reduced the late sustained LPP response, whereas the FA induction enhanced the LPP.</p></div><div><h3>Conclusions</h3><p>Acute manipulation of OM and FA states may reduce and enhance motivated attention to aversive stimuli during conditions of high subjective arousal, respectively. Functional distinctions between different mindfulness states on emotion processing may be most dissociable after accounting for within-participant variability in how stimuli are appraised. These results support the future potential of the state induction protocol for parsing the neural affective mechanisms that underlie mindfulness training programs and interventions.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100357"},"PeriodicalIF":4.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000703/pdfft?md5=aee0b80cfe093e2bc520c3ceb00ea55e&pid=1-s2.0-S2667174324000703-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141950436","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":"Potential Inflammatory Markers Related to the Conversion to Alzheimer’s Disease in Female Patients With Late-Life Depression","authors":"Jee Hyung Pyo ,&nbsp;Sae Saem Han ,&nbsp;Min-Ji Kim ,&nbsp;Young Kyung Moon ,&nbsp;Su Jin Lee ,&nbsp;Chaemin Lee ,&nbsp;AhRam Lee ,&nbsp;Shinn-Won Lim ,&nbsp;Doh Kwan Kim","doi":"10.1016/j.bpsgos.2024.100356","DOIUrl":"10.1016/j.bpsgos.2024.100356","url":null,"abstract":"<div><h3>Background</h3><p>Inflammation has been postulated as a mediating factor in the development of Alzheimer’s disease (AD) pathology. We investigated candidate inflammatory markers related to conversion to AD among patients with depression.</p></div><div><h3>Methods</h3><p>A longitudinal study was conducted with older women with depression who were at least 55 years of age, with a mean follow-up period of 5.73 years. At baseline, 9 inflammatory cytokines were measured using the immunoreactivity method. During follow-up, patients with depression who complained of cognitive impairment were evaluated and diagnosed with AD conversion. Association of the cytokines with conversion to AD was analyzed using multivariable Cox proportional hazards regression with adjusting covariates. For clinical applicability, the optimal cutoff value was determined using the minimum <em>p</em> value approach for the conversion to AD and was used to plot an AD-free survival curve.</p></div><div><h3>Results</h3><p>Among 132 participants, 34 patients with depression (25.76%) developed AD during their follow-up period. Higher levels of interleukin (IL) 1β at baseline (hazard ratio = 3.30 [95% CI, 1.11–9.78], <em>p</em> = .031) and lower levels of IL-10 (<em>p</em> &lt; .001) were significantly associated with an increased risk of progression to AD. The survival curve plotted by the cutoff value of ≥0.25 pg/mL for IL-1β and ≤0.15 pg/mL for IL-10 suggested adjusted hazard ratios of 8.96 (95% CI, 3.48–23.09; <em>p</em> &lt; .001) for IL-1β and 10.99 (<em>p</em> &lt; .001) for IL-10, respectively.</p></div><div><h3>Conclusions</h3><p>This study demonstrated that IL-1β and IL-10 were associated with conversion to AD among patients with late-life depression, suggesting their potential as predictive markers of the transition to AD from depression.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100356"},"PeriodicalIF":4.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000697/pdfft?md5=993afd834df8b58554a2a64cfa6aa50b&pid=1-s2.0-S2667174324000697-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141962466","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":"Altered Physiological, Affective, and Functional Connectivity Responses to Acute Stress in Patients With Alcohol Use Disorder","authors":"Yana Schwarze ,&nbsp;Johanna Voges ,&nbsp;Alexander Schröder ,&nbsp;Sven Dreeßen ,&nbsp;Oliver Voß ,&nbsp;Sören Krach ,&nbsp;Frieder Michel Paulus ,&nbsp;Klaus Junghanns ,&nbsp;Lena Rademacher","doi":"10.1016/j.bpsgos.2024.100358","DOIUrl":"10.1016/j.bpsgos.2024.100358","url":null,"abstract":"<div><h3>Background</h3><p>There is evidence that the processing of acute stress is altered in alcohol use disorder (AUD), but little is known about how this is manifested simultaneously across different stress parameters and which neural processes are involved. The current study examined physiological and affective responses to stress and functional connectivity in AUD.</p></div><div><h3>Methods</h3><p>Salivary cortisol samples, pulse rate, and affect ratings were collected on 2 days from 34 individuals with moderate or severe AUD during early abstinence and 34 control participants. On one of the days, stress was induced, and on the other day, a nonstressful control task was performed. Following the intervention, participants underwent functional magnetic resonance imaging to assess functional connectivity, with a focus on cortical and subcortical seed regions previously reported to be involved in AUD and/or stress.</p></div><div><h3>Results</h3><p>For pulse rate and cortisol, stress responses were blunted in AUD, whereas the affective response was stronger. Neuroimaging analyses revealed stress-related group differences in functional connectivity, involving the connectivity of striatal seeds with the posterior default mode network, cerebellum, and midcingulate cortex and of the posterior default mode network seed with the striatum and thalamus.</p></div><div><h3>Conclusions</h3><p>The results suggest a dissociation between subjectively experienced distress and the physiological stress response in AUD as well as stress-related alterations in functional connectivity. These findings highlight the complex interplay between chronic alcohol use and acute stress regulation, offering valuable considerations for the development of therapeutic strategies.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100358"},"PeriodicalIF":4.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000715/pdfft?md5=829d23d3959b36a21224f1f93edf4cbc&pid=1-s2.0-S2667174324000715-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141950421","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":"NEGR1 Modulates Mouse Affective Discrimination by Regulating Adult Olfactory Neurogenesis","authors":"Kwang Hwan Kim ,&nbsp;Kyungchul Noh ,&nbsp;Jaesung Lee ,&nbsp;Soojin Lee ,&nbsp;Sung Joong Lee","doi":"10.1016/j.bpsgos.2024.100355","DOIUrl":"10.1016/j.bpsgos.2024.100355","url":null,"abstract":"<div><h3>Background</h3><p>Affective recognition and sensory processing are impaired in people with autism. However, no mouse model of autism comanifesting these symptoms is available, thereby limiting the exploration of the relationship between affective recognition and sensory processing in autism and the molecular mechanisms involved.</p></div><div><h3>Methods</h3><p>With <em>Negr1</em>^−/− mice, we conducted the affective state discrimination test and an odor habituation/dishabituation test. Data were analyzed using the <em>k</em>-means clustering method. We also employed a whole-cell patch clamp and bromodeoxyuridine incorporation assay to investigate underlying mechanisms.</p></div><div><h3>Results</h3><p>When encountering mice exposed to restraint stress or chronic pain, wild-type mice discriminated between them by either approaching the stressed mouse or avoiding the painful mouse, whereas <em>Negr1</em>^−/− mice showed unbiased social interactions with them. Next, we demonstrated that both wild-type and <em>Negr1</em>^−/− mice used their olfaction for social interaction in the experimental context, but <em>Negr1</em>^−/− mice showed aberrant olfactory habituation and dishabituation against social odors. In electrophysiological studies, inhibitory inputs to the mitral cells in the olfactory bulb were increased in <em>Negr1</em>^−/− mice compared with wild-type mice, and subsequently their excitability was decreased. As a potential underlying mechanism, we found that adult neurogenesis in the subventricular zone was diminished in <em>Negr1</em>^−/− mice, which resulted in decreased integration of newly generated inhibitory neurons in the olfactory bulb.</p></div><div><h3>Conclusions</h3><p>NEGR1 contributes to mouse affective recognition, possibly by regulating olfactory neurogenesis and subsequent olfactory sensory processing. We propose a novel neurobiological mechanism of autism-related behaviors based on disrupted adult olfactory neurogenesis.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100355"},"PeriodicalIF":4.0,"publicationDate":"2024-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000685/pdfft?md5=3047facdeec4d46893952541055234f7&pid=1-s2.0-S2667174324000685-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141954329","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":"Genetic Implication of Specific Glutamatergic Neurons of the Prefrontal Cortex in the Pathophysiology of Schizophrenia","authors":"Claire E. Tume ,&nbsp;Sophie L. Chick ,&nbsp;Peter A. Holmans ,&nbsp;Elliott Rees ,&nbsp;Michael C. O’Donovan ,&nbsp;Darren Cameron ,&nbsp;Nicholas J. Bray","doi":"10.1016/j.bpsgos.2024.100345","DOIUrl":"10.1016/j.bpsgos.2024.100345","url":null,"abstract":"<div><h3>Background</h3><p>The prefrontal cortex (PFC) has been strongly implicated in the pathophysiology of schizophrenia. Here, we combined high-resolution single-nuclei RNA sequencing data from the human PFC with large-scale genomic data for schizophrenia to identify constituent cell populations likely to mediate genetic liability to the disorder.</p></div><div><h3>Methods</h3><p>Gene expression specificity values were calculated from a single-nuclei RNA sequencing dataset comprising 84 cell populations from the human PFC, spanning gestation to adulthood. Enrichment of schizophrenia common variant liability and burden of rare protein-truncating coding variants were tested in genes with high expression specificity for each cell type. We also explored schizophrenia common variant associations in relation to gene expression across the developmental trajectory of implicated neurons.</p></div><div><h3>Results</h3><p>Common risk variation for schizophrenia was prominently enriched in genes with high expression specificity for a population of mature layer 4 glutamatergic neurons emerging in infancy. Common variant liability to schizophrenia increased along the developmental trajectory of this neuronal population. Fine-mapped genes at schizophrenia genome-wide association study risk loci had significantly higher expression specificity than other genes in these neurons and in a population of layer 5/6 glutamatergic neurons. People with schizophrenia had a higher rate of rare protein-truncating coding variants in genes expressed by cells of the PFC than control individuals, but no cell population was significantly enriched above this background rate.</p></div><div><h3>Conclusions</h3><p>We identified a population of layer 4 glutamatergic PFC neurons likely to be particularly affected by common variant genetic risk for schizophrenia, which may contribute to disturbances in thalamocortical connectivity in the condition.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100345"},"PeriodicalIF":4.0,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000582/pdfft?md5=f641cddd1fec59a688d4fd7e2c5823bc&pid=1-s2.0-S2667174324000582-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141409295","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":"11.7T Diffusion Magnetic Resonance Imaging and Tractography to Probe Human Brain Organoid Microstructure","authors":"","doi":"10.1016/j.bpsgos.2024.100344","DOIUrl":"10.1016/j.bpsgos.2024.100344","url":null,"abstract":"<div><h3>Background</h3><p>Human brain organoids are 3-dimensional cellular models that mimic architectural features of a developing brain. Generated from human induced pluripotent stem cells, these organoids offer an unparalleled physiologically relevant in vitro system for disease modeling and drug screening. In the current study, we sought to establish a foundation for a magnetic resonance imaging (MRI)–based, label-free imaging system that offers high-resolution capabilities for deep tissue imaging of whole organoids.</p></div><div><h3>Methods</h3><p>An 11.7T Bruker/89 mm microimaging system was used to collect high-resolution multishell 3-dimensional diffusion images of 2 induced pluripotent stem cell–derived human hippocampal brain organoids. The MRI features identified in the study were interpreted on the basis of similarities with immunofluorescence microscopy.</p></div><div><h3>Results</h3><p>MRI microscopy at ≤40 μm isotropic resolution provided a 3-dimensional view of organoid microstructure. T2-weighted contrast showed a rosette-like internal structure and a protruding spherical structure that correlated with immunofluorescence staining for the choroid plexus. Diffusion tractography methods can be used to model tissue microstructural features and possibly map neuronal organization. This approach complements traditional immunohistochemistry imaging methods without the need for tissue clearing.</p></div><div><h3>Conclusions</h3><p>This proof-of-concept study shows, for the first time, the application of high-resolution diffusion MRI microscopy to image 2-mm diameter spherical human brain organoids. Application of ultrahigh-field MRI and diffusion tractography is a powerful modality for whole organoid imaging and has the potential to make a significant impact for probing microstructural changes in brain organoids used to model psychiatric disorders, neurodegenerative diseases, and viral infections of the human brain, as well as for assessing neurotoxicity in drug screening.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100344"},"PeriodicalIF":4.0,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000570/pdfft?md5=1c228c71c00dd68d6142cd5f57c044fb&pid=1-s2.0-S2667174324000570-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141401165","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}