Biological psychiatry. Cognitive neuroscience and neuroimaging最新文献

{"title":"Neurite Density and Kurtosis in the Gray Matter of People with Early Schizophrenia.","authors":"Peter C Van Dyken, Ali R Khan, Lena Palaniyappan","doi":"10.1016/j.bpsc.2025.06.001","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.06.001","url":null,"abstract":"<p><strong>Background: </strong>Classical models of diffusion weighted imaging, especially diffusion tensor imaging, are unsuited for application to the cortical gray matter, given the regions high microstructural complexity. As such, most neuroimaging studies thus far have focused on gross structural effects of schizophrenia, such as cortical thickness differences. More recently developed models, such as the neurite orientation dispersion and density imaging (NODDI) model and diffusion kurtosis imaging (DKI), incorporate higher resolution data and may provide more sensitive descriptions of schizophrenia pathology with more specific interpretations.</p><p><strong>Methods: </strong>We applied the NODDI and DKI models to the cortical gray matter of people with early schizophrenia (n=54) and healthy controls (n=51) from the Human Connectome Project - Early Psychosis dataset. Comparisons between groups were made using region-of-interest and clustering approaches. The effect sizes of these approaches were compared to those of cortical thickness differences. We also investigated the relationship between these parameters and lifetime antipsychotic usage.</p><p><strong>Results: </strong>Cortical thickness differences were most prominent between groups in terms of global effect size and spatial extent. We also observed a diffuse, right-hemisphere dominant increase in mean kurtosis and isotropic diffusion fraction throughout the gray matter, not fully explained by partial volume effects. Additionally, a lower neurite density index (NDI) correlated with greater lifetime antipsychotic usage.</p><p><strong>Conclusions: </strong>Increases in mean kurtosis and isotropic diffusion fraction are both markers of schizophrenia, consistent with inflammation models of the gray matter in schizophrenia. NDI reduction, reflecting intraneurite pathology, becomes prominent only in those with greater disease burden.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144287534","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":"Cerebello-Thalamo-Cortical Dysconnectivity in Schizophrenia Spectrum Disorders: A Resting-State fMRI Meta-Analysis.","authors":"Orsolya Lányi, Daniel Zahemszky, Alexander Schulze Wenning, Marie Anne Engh, Zsolt Molnár, András Attila Horváth, Péter Hegyi, Gábor Csukly","doi":"10.1016/j.bpsc.2025.05.017","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.017","url":null,"abstract":"<p><strong>Background: </strong>Cerebello-thalamo-cortical (CTC) network dysfunctions are well-documented in schizophrenia spectrum disorders (SSD) and preclinical states. However, small samples and methodological heterogeneity often limit individual neuroimaging studies. To overcome these challenges, we conducted a coordinate-based meta-analysis to characterize CTC alterations across illness stages and examine associations with symptom dimensions.</p><p><strong>Methods: </strong>Our meta-analysis was preregistered and followed the PRISMA guideline and the recommendations of the Cochrane Handbook. A systematic search was conducted in three databases in September 2023. Included articles used seed-based resting-state fMRI in patients with schizophrenia-spectrum disorders, first-episode psychosis, clinical high-risk for psychosis, and healthy control groups. Seeds were defined in the thalamus and the cerebellum. Two coordinate-based meta-analytic methods, Activation Likelihood Estimation and Seed-based D Mapping were used. Risk of bias was evaluated per the OHBM recommendations.</p><p><strong>Results: </strong>Thalamic hypoconnectivity in the prefrontal cortex, limbic lobe, thalamus and the cerebellum, and hyperconnectivity in the somato-motor and visual association areas was found in SSD (29 studies, 2768 patients). Dysconnectivity was linked to disease progression and symptoms. Cerebellar analysis indicated hypoconnectivity in the prefrontal cortex, cerebellum, and thalamus, with hyperconnectivity in the motor cortex, somatosensory cortex, and orbitofrontal cortex (19 studies, 1159 patients). Cerebellar clusters did not survive multiple comparison correction.</p><p><strong>Conclusions: </strong>Our findings provide robust meta-analytic evidence of cerebello-thalamo-cortical dysconnectivity in SSD, suggesting this network captures a core neurobiological feature of psychotic disorders. Consistent patterns of altered CTC connectivity underscore the importance of future clinical investigations of this network as a potential target for therapeutic interventions.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144277041","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":"Auditory and Visual Thalamocortical Connectivity Alterations in Unmedicated People with Schizophrenia: An Individualized Sensory Thalamic Localization and Resting-State Functional Connectivity Study.","authors":"John C Williams, Philip N Tubiolo, Roberto B Gil, Zu Jie Zheng, Eilon B Silver-Frankel, Natalka K Haubold, Sameera K Abeykoon, Dathy T Pham, Najate Ojeil, Kelly Bobchin, Mark Slifstein, Jodi J Weinstein, Greg Perlman, Guillermo Horga, Anissa Abi-Dargham, Jared X Van Snellenberg","doi":"10.1016/j.bpsc.2025.05.016","DOIUrl":"10.1016/j.bpsc.2025.05.016","url":null,"abstract":"<p><strong>Background: </strong>Converging evidence from clinical neuroimaging and animal models has strongly implicated dysfunction of thalamocortical circuits in the pathophysiology of schizophrenia. Preclinical models of genetic risk for schizophrenia have shown reduced synaptic transmission from auditory thalamus to primary auditory cortex, which may represent a correlate of auditory disturbances such as hallucinations. Human neuroimaging studies, however, have found a generalized increase in resting state functional connectivity (RSFC) between whole thalamus and sensorimotor cortex in people with schizophrenia (PSZ). We aimed to more directly translate preclinical findings by specifically localizing auditory and visual thalamic nuclei in unmedicated PSZ and measuring RSFC to primary sensory cortices.</p><p><strong>Methods: </strong>In this case-control study, 82 unmedicated PSZ and 55 matched healthy controls (HC) completed RSFC functional magnetic resonance imaging (fMRI). Auditory and visual thalamic nuclei were localized for 55 unmedicated PSZ and 46 HC who additionally completed a sensory thalamic nuclei localizer fMRI task (N = 101). Using localized nuclei as RSFC seeds we assessed group differences in auditory and visual thalamocortical connectivity and associations with positive symptom severity.</p><p><strong>Results: </strong>Auditory thalamocortical connectivity was not significantly different between PSZ and HC, but hyperconnectivity was associated with greater positive symptom severity in bilateral superior temporal gyrus. Visual thalamocortical connectivity was significantly greater in PSZ relative to HC in secondary and higher-order visual cortex, but not predictive of positive symptom severity.</p><p><strong>Conclusion: </strong>These results indicate that visual thalamocortical hyperconnectivity is a generalized marker of schizophrenia, while hyperconnectivity in auditory thalamocortical circuits relates more specifically to positive symptom severity.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251295","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 Neural Spectrum of Disturbed Emotion.","authors":"Maurizio Sicorello","doi":"10.1016/j.bpsc.2025.05.014","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.014","url":null,"abstract":"","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144210478","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":"Face Processing in School-Aged Preterm Children: Assessing Neural Sensitivity to Facial Identity and Expression Using Frequency-Tagging EEG.","authors":"Tiffany Tang, Matthijs Moerkerke, Nicky Daniels, Stephanie Van der Donck, Jean Steyaert, Gunnar Naulaers, Kaat Alaerts, Els Ortibus, Bart Boets","doi":"10.1016/j.bpsc.2025.05.015","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.015","url":null,"abstract":"<p><strong>Background: </strong>Preterm (PT) birth is associated with important social vulnerabilities that can have long-term implications and may result in psychopathology (e.g., autism spectrum disorder). A recurring \"preterm behavioral phenotype\" has been described, although these difficulties may often be subtle and subclinical. As face processing is crucial for social interactions and several studies reported impaired face processing performance in PT populations, we hypothesize that face processing difficulties may contribute to or be a part of these social difficulties. Here, we investigate the neural sensitivity for crucial socio-communicative facial cues in school-aged PT children.</p><p><strong>Methods: </strong>Thirty-nine 8-to-12-year-old PT children born between 24 and 32 weeks of gestation and thirty-eight term-born matched controls performed a series of innovative facial identity and expression discrimination frequency-tagging electroencephalography paradigms. More specifically, we evaluated the neural sensitivity to implicitly and automatically discriminate a different facial identity among a stream of identical faces, as well as an expressive face (fearful and happy, in separate sequences) among a stream of neutral faces.</p><p><strong>Results: </strong>We found intact implicit facial identity and expression processing in both groups. Unexpectedly, PT participants showed a significantly greater neural sensitivity towards these subtle socio-communicative facial cues. Correlations with neonatal measures such as gestational age and birth weight showed that this greater neural sensitivity is uniformly present among the PT group.</p><p><strong>Conclusion: </strong>Evidence suggests that impaired neural sensitivity for facial cues may not be the primary cause for behavioral face processing and social difficulties often encountered in PT children.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144210477","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":"Granularity of emotions in brain and behavior and resilience to childhood violence exposure.","authors":"David G Weissman, Shafi Rubbani, Stephanie N DeCross, Steven W Kasparek, Katie A McLaughlin","doi":"10.1016/j.bpsc.2025.05.012","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.012","url":null,"abstract":"<p><strong>Background: </strong>This study identified behavioral and neural indices of the specificity of emotion representations in adolescents' brains and assessed their association with resilience to childhood violence exposure.</p><p><strong>Methods: </strong>Eighty 13-18-year-old adolescents with variable exposure to violence viewed emotion-eliciting videos and rated how angry, disgusted, sad, scared, and upset they felt. Sixty-nine participants viewed the same videos in the MRI scanner, once while labelling their emotions and once while counting the number of people.</p><p><strong>Results: </strong>Emotion labelling (vs. counting) led to greater BOLD activation in medial and ventrolateral prefrontal cortex. Based on RSA, if two stimuli elicited more similar patterns of activation within those brain regions, those stimuli had more similar emotion ratings, suggesting that encoding of emotion categories within these brain regions is reflected in their activation patterns. Moreover, emotion differentiation measured behaviorally and the mean neural dissimilarity across all stimulus pairs for each participant each moderated the association between violence exposure and psychopathology, such that the association between violence exposure and psychopathology was weaker in those with greater emotion differentiation and neural dissimilarity.</p><p><strong>Conclusions: </strong>The granularity of emotions reflected in adolescents' brains and behavior contribute to resilience and therefore may serve as a target for preventative interventions.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144188677","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":"Computationally-informed insights into anhedonia and treatment by k-opioid receptor antagonism.","authors":"Bilal A Bari, Andrew D Krystal, Diego A Pizzagalli, Samuel J Gershman","doi":"10.1016/j.bpsc.2025.05.011","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.011","url":null,"abstract":"<p><strong>Background: </strong>Anhedonia, the loss of pleasure, is prevalent and impairing. Parsing its computational basis promises to explain its transdiagnostic character. One manifestation of anhedonia-reward insensitivity-may be linked to limited memory. Further, the need to economize on limited memory engenders a perseverative bias towards frequently chosen actions. Anhedonia may also be linked with deviations from optimal perseveration for a given memory capacity, a pattern that causes inefficiency because it results in less reward for the same memory cost.</p><p><strong>Methods: </strong>To test these hypotheses, we apply a theory of optimal decision-making under memory constraints that decomposes behavior into a memory component and an efficiency component. We apply this theory to behavior on the Probabilistic Reward Task, a reward learning paradigm validated in anhedonia, and perform secondary analysis of a randomized controlled trial testing κ-opioid receptor (KOR) antagonism for anhedonia (N=24 KOR; N=31 placebo), as well as analyses of three other datasets (N=100, 66, 24 respectively). We fit a resource-bounded reinforcement-learning model to behavior.</p><p><strong>Results: </strong>Across clinical and nonclinical populations, anhedonia is associated with deficits in efficiency but not memory. The reinforcement learning models demonstrate that deficits in efficiency arise from the inability to perseverate optimally. KOR antagonism, which likely elevates tonic dopamine, increases both memory and efficiency, and the model demonstrates that this arises from increased reward sensitivity and perseveration.</p><p><strong>Conclusions: </strong>KOR antagonism therefore has distinct cognitive effects, only one related to anhedonia. These findings have potential implications for the applications of KOR antagonists.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144188676","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":"Penetrance of neurodevelopmental copy number variants is associated with variations in cortical morphology.","authors":"Ana I Silva, Ida E Sønderby, George Kirov, Abdel Abdellaoui, Ingrid Agartz, David Ames, Nicola J Armstrong, Eric Artiges, Tobias Banaschewski, Anne S Bassett, Carrie E Bearden, John Blangero, Rune Boen, Dorret I Boomsma, Robin Bülow, Nancy J Butcher, Vince Calhoun, Linda E Campbell, Eva W C Chow, Simone Ciufolini, Michael C Craig, Benedicto Crespo-Farroco, Adam C Cunningham, Shareefa Dalvie, Eileen Daly, Paola Dazzan, Eco J C de Geus, Greig I de Zubicaray, Joanne L Doherty, Gary Donohoe, Mark Drakesmith, Thomas Espeseth, Vincent Frouin, Hugh Garavan, David C Glahn, Naomi J Goodrich-Hunsaker, Penny A Gowland, Hans J Grabe, Antoine Grigis, Maria Gudbrandsen, Boris A Gutman, Jan Haavik, Asta K Håberg, Jeremy Hall, Andreas Heinz, Sarah Hohmann, Jouke-Jan Hottenga, Sébastien Jacquemont, Neda Jahanshad, Rachel K Jonas, Derek K Jones, Erik G Jönsson, Sanne Koops, Kuldeep Kumar, Stephanie Le Hellard, Herve Lemaitre, Jingyu Liu, Astri J Lundervold, Jean-Luc Martinot, Karen A Mather, Donna M McDonald-McGinn, Katie L McMahon, Allan F McRae, Sarah E Medland, Clara A Moreau, Kieran C Murphy, Declan Murphy, Robin M Murray, Frauke Nees, Michael J Owen, Marie-Laure Paillère Martinot, Diimitri Papadopoulos Orfanos, Tomas Paus, Luise Poustka, Tiago Reis Marques, David R Roalf, Perminder S Sachdev, Freda Scheffler, J Eric Schmitt, Gunter Schumann, Vidar M Steen, Dan J Stein, Lachlan T Strike, Alexander Teumer, Anbupalam Thalamuthu, Sophia I Thomopoulos, Diana Tordesillas-Gutiérrez, Julian N Trollor, Anne Uhlmann, Ariana Vajdi, Dennis van 't Ent, Therese van Amelsvoort, Marianne B M van den Bree, Dennis van der Meer, Javier Vázquez-Bourgon, Julio E Villalón-Reina, Uwe Völker, Henry Völzke, Jacob A S Vorstman, Lars T Westlye, Nigel Williams, Katharina Wittfeld, Margaret J Wright, Paul M Thompson, Ole A Andreassen, David E J Linden","doi":"10.1016/j.bpsc.2025.05.010","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.010","url":null,"abstract":"<p><strong>Background: </strong>Copy number variants (CNVs) increase risk for neurodevelopmental conditions. The neurobiological mechanisms linking these high-risk genetic variants to clinical phenotypes are largely unknown. An important question is whether brain abnormalities in individuals carrying CNVs are associated with their degree of penetrance.</p><p><strong>Methods: </strong>We investigated if increased CNV-penetrance for schizophrenia and other developmental disorders was associated with variations in cortical and subcortical morphology. We pooled T1-weighted brain magnetic resonance imaging and genetic data from 22 cohorts from the ENIGMA-CNV consortium. In the main analyses, we included 9,268 individuals (aged 7 to 90 years, 54% females), from which we identified 398 carriers of 36 neurodevelopmental CNVs at 20 distinct loci. A secondary analysis was performed including additional neuroimaging data from the ENIGMA-22q consortium, including 274 carriers of the 22q11.2 deletion and 291 non-carriers. CNV-penetrance was estimated through penetrance scores that were previously generated from large cohorts of patients and controls. These scores represent the probability risk to develop either schizophrenia or other developmental disorders (including developmental delay, autism spectrum disorder and congenital malformations).</p><p><strong>Results: </strong>For both schizophrenia and developmental disorders, increased penetrance scores were associated with lower surface area in the cerebral cortex and lower intracranial volume. For both conditions, associations between CNV-penetrance scores and cortical surface area were strongest in regions of the occipital lobes, specifically in the cuneus and lingual gyrus.</p><p><strong>Conclusions: </strong>Our findings link global and regional cortical morphometric features with CNV-penetrance, providing new insights into neurobiological mechanisms of genetic risk for schizophrenia and other developmental disorders.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144868","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":"Visual Deficits in Contrast and Depth Perception in Psychotic Disorders: Implications for a Neural Hierarchy.","authors":"Baktash Babadi, Daphne J Holt, Roger B H Tootell","doi":"10.1016/j.bpsc.2025.05.009","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.009","url":null,"abstract":"<p><strong>Background: </strong>A key challenge in understanding the neurobehavioral mechanisms of psychotic disorders (PD) is identifying the level and interactions of the affected brain regions. The early visual system, with its hierarchical structure, offers a model for studying such mechanisms. Specifically, variations in visual contrast are detected as early as in the retina, whereas binocular depth perception emerges at a higher level, in visual cortex. Comparing these processes within individuals can provide insights into the mechanisms and progression of perceptual deficits in PD.</p><p><strong>Methods: </strong>Psychophysical sensitivity to stimulus contrast and binocular disparity were assessed in 53 PD subjects and 58 demographically-matched healthy control (HC) subjects. Across the two tasks, the physical features of the stimuli were matched except for the primary variable of interest. Psychometric functions were fitted to the performance of each subject, and the normalized area under the psychometric curves quantified the average performance across stimulus strengths.</p><p><strong>Results: </strong>The PD group showed significantly impaired performance in both visual contrast detection (p<0.007) and binocular depth perception (p<0.021), compared to the HC group. In the PD but not the HC group, the performance across the two tasks were correlated with each other. A direct comparison revealed a more pronounced deficit in depth perception compared to contrast detection in the PD group. Differences in psychometric parameters (i.e. threshold, flatness, and lapse rate) revealed additional cognitive and attentional dysfunctions in the PD group.</p><p><strong>Conclusion: </strong>These findings provide evidence for a progressive accumulation of deficits through the visual hierarchy in psychosis.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144871","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":"Neural Response to Reward and Loss Following Basic Combat Training.","authors":"Clara Freeman, Eric Rawls, Collin D Teich, Scott R Sponheim, Melissa A Polusny, Craig Marquardt","doi":"10.1016/j.bpsc.2025.05.007","DOIUrl":"https://doi.org/10.1016/j.bpsc.2025.05.007","url":null,"abstract":"<p><strong>Background: </strong>The brain's responsiveness to rewarding stimuli is essential for adaptive functioning while deficits in neural reward processing have been linked to the transdiagnostic symptom of anhedonia. Acute or prolonged stressors may negatively impact neural reward responses; however, few studies have examined if real-world naturalistic stressors prospectively predict reductions in brain responses to rewards.</p><p><strong>Methods: </strong>This pre-registered analysis (https://osf.io/f6e8w) used data from the ARMOR study to assess whether exposure to basic combat training (BCT), a demanding and stress-inducing 10-week program, led to reductions in electrophysiological measures of reward response. One hundred sixteen military recruits completed a virtual gambling task while electroencephalogram (EEG) was recorded before and after BCT. Mean EEG activity in the time window of the Reward Positivity (RewP; 175 - 325ms post-feedback at FCz) was averaged separately for the gain and loss condition.</p><p><strong>Results: </strong>We found that neural response to both gain and loss feedback in the time-window of the RewP significantly decreased from baseline following BCT (b = -0.67, p <.001), but the difference between conditions did not (b = 0.28, p = .23). Greater reports of BCT-related stressors predicted decreased neural response to gain, but not loss. Finally, baseline reward-related power in the delta-band frequency prospectively predicted less self-reported BCT-related stress.</p><p><strong>Conclusions: </strong>These findings suggest that experiencing the stress of BCT is associated with reductions in neural processing of both reward and loss feedback. Further, those with greater reward-related delta oscillatory activity may perceive less negative impact of real-world stressors.</p>","PeriodicalId":93900,"journal":{"name":"Biological psychiatry. Cognitive neuroscience and neuroimaging","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144867","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}