Biological Psychiatry-Cognitive Neuroscience and Neuroimaging最新文献

{"title":"An In Vivo Examination of the Relationship Between Metabotropic Glutamate 5 Receptor and Suicide Attempts in People With Borderline Personality Disorder","authors":"Margaret T. Davis ,&nbsp;Ruth H. Asch ,&nbsp;Emily R. Weiss ,&nbsp;Ashley Wagner ,&nbsp;Sarah K. Fineberg ,&nbsp;Nabeel Nabulsi ,&nbsp;David Matuskey ,&nbsp;Richard E. Carson ,&nbsp;Irina Esterlis","doi":"10.1016/j.bpsc.2024.11.014","DOIUrl":"10.1016/j.bpsc.2024.11.014","url":null,"abstract":"<div><h3>Background</h3><div>Borderline personality disorder (BPD) is a serious psychiatric condition that is associated with a high risk for suicide attempts (SAs) and death by suicide. However, relatively little is known about the pathophysiology of BPD. The metabotropic glutamate 5 receptor (mGlu₅) has been specifically implicated in the pathophysiology of BPD and SAs, with more general roles in emotion regulation, social and cognitive functioning, and pain processing. Here, we examined the relationship between mGlu₅ availability, BPD, and SAs in vivo for the first time.</div></div><div><h3>Methods</h3><div>Eighteen individuals with BPD, 18 healthy control participants matched on age, sex, and smoking status, and 18 clinical comparison control participants with major depressive disorder completed comprehensive clinical assessments and participated in an [¹⁸F]FPEB positron emission tomography scan to measure mGlu₅ availability. The volume of distribution (<em>V</em>_T) in the frontolimbic circuit implicated in BPD pathophysiology was the positron emission tomography outcome measure.</div></div><div><h3>Results</h3><div>We observed significantly higher frontolimbic mGlu₅ availability in the BPD group than in both the healthy control group (<em>p</em> = .009, <em>d</em> = 0.84, 18.43% difference) and the major depressive disorder group (<em>p</em> = .03, <em>d</em> = 0.69, 15.21% difference). In the BPD, but not the major depressive disorder group, higher mGlu₅ availability was also associated with a history of SAs (19–25% higher, <em>p</em>s = .02–.005). Furthermore, mGlu₅ availability was positively correlated with risk factors for suicide (e.g., sexual victimization, perceived burdensomeness) in individuals with BPD and a history of SA.</div></div><div><h3>Conclusions</h3><div>Results show higher mGlu₅ availability in BPD and SA for the first time. Our preliminary findings suggest that mGlu₅ may be a critical treatment target for BPD symptoms, including SAs, and warrant additional investigation in larger samples.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 324-332"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142756045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial Board Page","authors":"","doi":"10.1016/S2451-9022(25)00040-0","DOIUrl":"10.1016/S2451-9022(25)00040-0","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Page A1"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143552127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intranasal Insulin Increases Brain Glutathione and Enhances Antioxidant Capacity in Healthy Participants but Not in Those With Early Psychotic Disorders","authors":"Virginie-Anne Chouinard ,&nbsp;Wirya Feizi ,&nbsp;Xi Chen ,&nbsp;Boyu Ren ,&nbsp;Kathryn E. Lewandowski ,&nbsp;Jacey Anderson ,&nbsp;Steven Prete ,&nbsp;Emma Tusuzian ,&nbsp;Kyle Cuklanz ,&nbsp;Shuqin Zhou ,&nbsp;Paula Bolton ,&nbsp;Abigail Stein ,&nbsp;Bruce M. Cohen ,&nbsp;Fei Du ,&nbsp;Dost Öngür","doi":"10.1016/j.bpsc.2024.11.018","DOIUrl":"10.1016/j.bpsc.2024.11.018","url":null,"abstract":"<div><h3>Background</h3><div>We examined the acute effects of intranasal insulin on cognitive function and brain glutathione (GSH), a central factor in resistance to oxidative stress, in both participants with early psychosis and healthy control (HC) participants.</div></div><div><h3>Methods</h3><div>Twenty-one patients with early-stage psychotic disorders and 18 HC participants underwent magnetic resonance spectroscopy (MRS) scans and cognitive assessments before and after administration of intranasal insulin 40 IU. We conducted proton MRS (¹H-MRS) in the prefrontal cortex at 4T to measure GSH and glutamate metabolites. We assessed cognition using the Brief Assessment of Cognition in Schizophrenia symbol coding, digit sequencing, and verbal fluency tasks, in addition to the Stroop task.</div></div><div><h3>Results</h3><div>The mean (SD) age of participants was 25.7 (4.6) years; 51.3% were female. There were no significant group differences at baseline in age, sex, body mass index, homeostatic model assessment of insulin resistance (HOMA-IR), or cognition. Patients had higher baseline GSH (<em>p</em> &lt; .001) and glutamate (<em>p</em> = .007). After insulin administration, GSH increased in HC participants (mean change, 0.15; 95% CI 0.03 to 0.26; <em>p</em> = .015), but not in patients. Symbol coding improved in both patients (0.74; 95% CI 0.37 to 1.11; <em>p</em> &lt; .001) and HC participants (0.83; 95% CI 0.58 to 1.09; <em>p</em> &lt; .001), and verbal fluency improved in HC participants (0.43; 95% CI 0.14 to 0.72; <em>p</em> = .006). Lower baseline HOMA-IR was associated with greater change in GSH (coefficient −0.22; 95% CI −0.40 to −0.04; <em>p</em> = .017).</div></div><div><h3>Conclusions</h3><div>Intranasal insulin increased brain GSH in HC participants, but not in patients with early psychotic disorders. These novel findings demonstrate that intranasal insulin enhances antioxidant capacity and resilience to oxidative stress in HC individuals in contrast to an absent antioxidant response in those with early psychotic disorders.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 286-294"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic Status Modulates Global and Local Brain Age Estimates in Overweight and Obese Adults","authors":"Shalaila S. Haas ,&nbsp;Fahim Abbasi ,&nbsp;Kathleen Watson ,&nbsp;Thalia Robakis ,&nbsp;Alison Myoraku ,&nbsp;Sophia Frangou ,&nbsp;Natalie Rasgon","doi":"10.1016/j.bpsc.2024.11.017","DOIUrl":"10.1016/j.bpsc.2024.11.017","url":null,"abstract":"<div><h3>Background</h3><div>As people live longer, maintaining brain health becomes essential for extending health span and preserving independence. Brain degeneration and cognitive decline are major contributors to disability. In this study, we investigated how metabolic health influences the brain age gap estimate (brainAGE), which measures the difference between neuroimaging-predicted brain age and chronological age.</div></div><div><h3>Methods</h3><div>K-means clustering was applied to fasting metabolic markers including insulin, glucose, leptin, cortisol, triglycerides, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol, steady-state plasma glucose, and body mass index of 114 physically and cognitively healthy adults. The homeostatic model assessment for insulin resistance served as a reference. T1-weighted brain magnetic resonance imaging was used to calculate voxel-level and global brainAGE. Longitudinal data were available for 53 participants over a 3-year interval.</div></div><div><h3>Results</h3><div>K-means clustering divided the sample into 2 groups, those with favorable (<em>n</em> = 58) and those with suboptimal (<em>n</em> = 56) metabolic health. The suboptimal group showed signs of insulin resistance and dyslipidemia (false discovery rate–corrected <em>p</em> &lt; .05) and had older global brainAGE and local brainAGE, with deviations most prominent in cerebellar, ventromedial prefrontal, and medial temporal regions (familywise error–corrected <em>p</em> &lt; .05). Longitudinal analysis revealed group differences but no significant time or interaction effects on brainAGE measures.</div></div><div><h3>Conclusions</h3><div>Suboptimal metabolic status is linked to accelerated brain aging, particularly in brain regions rich in insulin receptors. These findings highlight the importance of metabolic health in maintaining brain function and suggest that promoting metabolic well-being may help extend health span.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 278-285"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Guide for Authors","authors":"","doi":"10.1016/S2451-9022(25)00044-8","DOIUrl":"10.1016/S2451-9022(25)00044-8","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages A5-A10"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143552130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolism Matters in Mental Health","authors":"Zachary Freyberg ,&nbsp;Judith M. Ford ,&nbsp;Mary L. Phillips","doi":"10.1016/j.bpsc.2024.12.009","DOIUrl":"10.1016/j.bpsc.2024.12.009","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 239-240"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143552132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional Connectivity Between Glutamate Receptor Antagonism and Insulin Pathways: Implications for Modeling Mechanism of Action of Ketamine/Esketamine and Dextromethorphan in Depression Treatment","authors":"Sabrina Wong ,&nbsp;Gia Han Le ,&nbsp;Rodrigo B. Mansur ,&nbsp;Joshua D. Rosenblat ,&nbsp;Roger S. McIntyre","doi":"10.1016/j.bpsc.2024.10.004","DOIUrl":"10.1016/j.bpsc.2024.10.004","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 241-243"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linking Mitochondrial Dysfunction, Neurotransmitter, and Neural Network Abnormalities and Mania: Elucidating Neurobiological Mechanisms of the Therapeutic Effect of the Ketogenic Diet in Bipolar Disorder","authors":"Zachary Freyberg ,&nbsp;Ana C. Andreazza ,&nbsp;Colleen A. McClung ,&nbsp;Mary L. Phillips","doi":"10.1016/j.bpsc.2024.07.011","DOIUrl":"10.1016/j.bpsc.2024.07.011","url":null,"abstract":"<div><div>There is growing interest in the ketogenic diet as a treatment for bipolar disorder (BD), and there are promising anecdotal and small case study reports of efficacy. However, the neurobiological mechanisms by which diet-induced ketosis might ameliorate BD symptoms remain to be determined, particularly in manic and hypomanic states—defining features of BD. Identifying these mechanisms will provide new markers to guide personalized interventions and provide targets for novel treatment developments for individuals with BD. In this critical review, we describe recent findings highlighting 2 types of neurobiological abnormalities in BD: 1) mitochondrial dysfunction and 2) neurotransmitter and neural network functional abnormalities. We link these abnormalities to mania/hypomania and depression in BD and then describe the biological underpinnings by which the ketogenic diet may have a beneficial effect in individuals with BD. We end the review by describing approaches that can be employed in future studies to elucidate the neurobiology that underlies the therapeutic effect of the ketogenic diet in BD. Doing this may provide marker predictors to identify individuals who will respond well to the ketogenic diet, as well as offer neural targets for novel treatment developments for BD.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 267-277"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141763219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reward Neurocircuitry Predicts Longitudinal Changes in Alcohol Use Following Trauma Exposure","authors":"Cecilia A. Hinojosa ,&nbsp;Sanne J.H. van Rooij ,&nbsp;Negar Fani ,&nbsp;Robyn A. Ellis ,&nbsp;Nathaniel G. Harnett ,&nbsp;Lauren A.M. Lebois ,&nbsp;Timothy D. Ely ,&nbsp;Tanja Jovanovic ,&nbsp;Vishnu P. Murty ,&nbsp;Stacey L. House ,&nbsp;Francesca L. Beaudoin ,&nbsp;Xinming An ,&nbsp;Thomas C. Neylan ,&nbsp;Gari D. Clifford ,&nbsp;Sarah D. Linnstaedt ,&nbsp;Laura T. Germine ,&nbsp;Scott L. Rauch ,&nbsp;John P. Haran ,&nbsp;Alan B. Storrow ,&nbsp;Christopher Lewandowski ,&nbsp;Jennifer S. Stevens","doi":"10.1016/j.bpsc.2024.09.015","DOIUrl":"10.1016/j.bpsc.2024.09.015","url":null,"abstract":"<div><h3>Background</h3><div>Trauma is a risk factor for developing maladaptive alcohol use. Preclinical research has shown that stress alters the processing of midbrain and striatal reward and incentive signals. However, little research has been conducted on alterations in reward-related neurocircuitry posttrauma in humans. Neuroimaging markers may be particularly useful because they can provide insight into the mechanisms that may make an individual vulnerable to developing trauma-related psychopathologies. In this study, we aimed to identify reward-related neural correlates associated with changes in alcohol use after trauma exposure.</div></div><div><h3>Methods</h3><div>Participants were recruited from U.S. emergency departments for the AURORA study (<em>n</em> = 286; 178 female). Trauma-related change in alcohol use at 8 weeks posttrauma relative to pretrauma was quantified as a change in 30-day total drinking per the PhenX Toolkit Alcohol 30-Day Quantity and Frequency measure. Reward-related neurocircuitry activation and functional connectivity were assessed 2 weeks posttrauma using functional magnetic resonance imaging during a monetary reward task using region of interest and whole-brain voxelwise analyses.</div></div><div><h3>Results</h3><div>Greater increase in alcohol use from pretrauma to 8 weeks posttrauma was predicted by 1) greater ventral tegmental area, 2) greater cerebellum activation during gain &gt; loss trials measured 2 weeks posttrauma, and 3) greater seed-based functional connectivity between the ventral tegmental area and lateral occipital cortex and precuneus.</div></div><div><h3>Conclusions</h3><div>Altered ventral tegmental area activation and functional connectivity early posttrauma may be associated with reward seeking and processing, thereby contributing to greater alcohol use posttrauma. These data provide novel evidence of neural correlates that underlie increased alcohol use early posttrauma that may be targeted via early interventions to prevent the development of maladaptive alcohol use.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 314-323"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antipsychotic-Induced Dysregulation of Glucose Metabolism Through the Central Nervous System: A Scoping Review of Animal Models","authors":"Emily Au ,&nbsp;Kristoffer J. Panganiban ,&nbsp;Sally Wu ,&nbsp;Kira Sun ,&nbsp;Bailey Humber ,&nbsp;Gary Remington ,&nbsp;Sri Mahavir Agarwal ,&nbsp;Adria Giacca ,&nbsp;Sandra Pereira ,&nbsp;Margaret Hahn","doi":"10.1016/j.bpsc.2024.10.001","DOIUrl":"10.1016/j.bpsc.2024.10.001","url":null,"abstract":"<div><div>The use of antipsychotic drugs is associated with adverse metabolic effects. Disruptions in glucose metabolism such as hyperglycemia and insulin resistance have been shown to occur with antipsychotic use, independent of changes in body weight or adiposity. The regulation of whole-body glucose metabolism is partly mediated by the central nervous system. In particular, the hypothalamus and brainstem are responsive to peripheral energy signals and subsequently mediate feedback mechanisms to maintain peripheral glucose homeostasis. In this scoping review of preclinical in vivo studies, we aimed to explore central mechanisms through which antipsychotics dysregulate glucose metabolism. A systematic search for animal studies identified 29 studies that met our eligibility criteria for qualitative synthesis. The studies suggest that antipsychotic-induced changes in autonomic nervous system activity, certain neurotransmitter systems, expression of neuropeptides, and central insulin action mediate impairments in glucose metabolism. These findings provide insight into potential targets for the mitigation of the adverse effects of antipsychotics on glucose metabolism.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"10 3","pages":"Pages 244-257"},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}