Pub Date : 2026-02-01DOI: 10.1016/j.bpsc.2025.09.023
Eleanna M. Melcher , Monica I. Duran , Gabriella M. Mamlouk , Leslie Christensen , Grace C. George , Amy J.H. Kind
Life-course social exposome exposures may influence structural neuroanatomy in early life, thereby altering risk and protective factors implicated in the biological mechanisms of disease. The literature examining geospatially defined early-life social exposome exposures and their association with structural neuroanatomy has not been characterized. A systematic search was conducted in PubMed, Scopus (Elsevier), Web of Science Core Collection (Clarivate), PsycINFO (EBSCO), and Google Scholar. The study team dually screened 4960 records, 35 of which were included in the final review. Most articles identified an association between adverse social exposome exposures and aberrant structural neuroanatomy (n = 32). Studies assessed multiple developmental periods: infancy (n = 4), childhood (n = 27), early adolescence (n = 11), and late adolescence (n = 7). The Area Deprivation Index was the most widely used social exposome metric (n = 21). Future research should seek harmonized approaches to investigating the duration and magnitude of exposures and their association with brain structure and function.
社会暴露可能影响生命早期的结构神经解剖学，从而改变与疾病生物学机制有关的风险和保护因素。研究地理空间定义的早期生活社会暴露及其与结构神经解剖学的关系的文献尚未被描述。系统检索PubMed、Scopus （Elsevier）、Web of Science Core Collection （Clarivate）、PsycINFO （EBSCO）和谷歌Scholar。研究小组对4960份记录进行了双重筛选，其中35份被纳入最终审查。大多数文章确定了不良社会暴露与异常结构神经解剖学之间的联系（n=32）。研究评估了多个发育阶段：婴儿期（n=4）、儿童期（n=27）、青春期早期（n=11）和青春期晚期（n=7）。区域剥夺指数（ADI）是最广泛使用的社会暴露度量（n= 21）。未来的研究应该寻求统一的方法来调查暴露的持续时间和程度以及它们与大脑结构和功能的关系。
{"title":"Geographic Measures of Early Life-Course Social Exposome in the Evaluation of Structural Neuroanatomy: A Scoping Review","authors":"Eleanna M. Melcher , Monica I. Duran , Gabriella M. Mamlouk , Leslie Christensen , Grace C. George , Amy J.H. Kind","doi":"10.1016/j.bpsc.2025.09.023","DOIUrl":"10.1016/j.bpsc.2025.09.023","url":null,"abstract":"<div><div>Life-course social exposome exposures may influence structural neuroanatomy in early life, thereby altering risk and protective factors implicated in the biological mechanisms of disease. The literature examining geospatially defined early-life social exposome exposures and their association with structural neuroanatomy has not been characterized. A systematic search was conducted in PubMed, Scopus (Elsevier), Web of Science Core Collection (Clarivate), PsycINFO (EBSCO), and Google Scholar. The study team dually screened 4960 records, 35 of which were included in the final review. Most articles identified an association between adverse social exposome exposures and aberrant structural neuroanatomy (<em>n</em> = 32). Studies assessed multiple developmental periods: infancy (<em>n</em> = 4), childhood (<em>n</em> = 27), early adolescence (<em>n</em> = 11), and late adolescence (<em>n</em> = 7). The Area Deprivation Index was the most widely used social exposome metric (<em>n</em> = 21). Future research should seek harmonized approaches to investigating the duration and magnitude of exposures and their association with brain structure and function.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 2","pages":"Pages 139-154"},"PeriodicalIF":4.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276948","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}
Pub Date : 2026-02-01DOI: 10.1016/j.bpsc.2025.12.009
Tarek K. Rajji
{"title":"Understanding the Older Brain in Depression","authors":"Tarek K. Rajji","doi":"10.1016/j.bpsc.2025.12.009","DOIUrl":"10.1016/j.bpsc.2025.12.009","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 2","pages":"Pages 137-138"},"PeriodicalIF":4.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146116499","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}
Pub Date : 2026-02-01DOI: 10.1016/j.bpsc.2025.12.004
Meryl A. Butters , Vonetta M. Dotson , Sara L. Weisenbach
{"title":"Depression and Executive Versus Processing Speed Impairment: The Challenge of Discernment","authors":"Meryl A. Butters , Vonetta M. Dotson , Sara L. Weisenbach","doi":"10.1016/j.bpsc.2025.12.004","DOIUrl":"10.1016/j.bpsc.2025.12.004","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 2","pages":"Pages 135-136"},"PeriodicalIF":4.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146116500","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}
Pub Date : 2026-02-01DOI: 10.1016/j.bpsc.2024.12.002
Rohit S. Kamath , Kimberly B. Weldon , Hannah R. Moser , Samantha A. Montoya , Kamar S. Abdullahi , Philip C. Burton , Scott R. Sponheim , Cheryl A. Olman , Michael-Paul Schallmo
Background
Contour integration, the process of joining spatially separated elements into a single unified line, has consistently been found to be impaired in schizophrenia. Recent work suggests that this deficit could be associated with psychotic symptomatology rather than a specific diagnosis such as schizophrenia.
Methods
Examining a transdiagnostic sample of participants with psychotic psychopathology, we obtained quantitative indices of contour perception in a psychophysical behavioral task. We also measured responses during an analogous task using ultra-high field (7T) functional magnetic resonance imaging (fMRI).
Results
We found impaired contour discrimination performance among people with psychotic psychopathology (PwPP) (n = 63) compared with healthy control participants (n = 34) and biological relatives of PwPP (n = 44). Participants with schizophrenia (n = 31) showed impaired task performance compared with participants with bipolar disorder (n = 18). fMRI showed higher responses in the lateral occipital cortex of PwPP than in control participants. Using task-based functional connectivity analyses, we observed abnormal connectivity between visual brain areas during contour perception among PwPP. These connectivity differences only emerged when participants had to distinguish the contour object from background distractors, suggesting that a failure to suppress noise elements relative to contour elements may underlie impaired contour processing in PwPP.
Conclusions
Our results are consistent with impaired contour integration in psychotic psychopathology, and especially schizophrenia, that is related to cognitive dysfunction and may be linked to impaired functional connectivity across visual regions.
{"title":"Impaired Contour Object Perception in Psychosis","authors":"Rohit S. Kamath , Kimberly B. Weldon , Hannah R. Moser , Samantha A. Montoya , Kamar S. Abdullahi , Philip C. Burton , Scott R. Sponheim , Cheryl A. Olman , Michael-Paul Schallmo","doi":"10.1016/j.bpsc.2024.12.002","DOIUrl":"10.1016/j.bpsc.2024.12.002","url":null,"abstract":"<div><h3>Background</h3><div><span>Contour integration, the process of joining spatially separated elements into a single unified line, has consistently been found to be impaired in schizophrenia. Recent work suggests that this deficit could be associated with psychotic </span>symptomatology rather than a specific diagnosis such as schizophrenia.</div></div><div><h3>Methods</h3><div>Examining a transdiagnostic sample of participants with psychotic psychopathology, we obtained quantitative indices of contour perception in a psychophysical behavioral task. We also measured responses during an analogous task using ultra-high field (7T) functional magnetic resonance imaging (fMRI).</div></div><div><h3>Results</h3><div>We found impaired contour discrimination performance among people with psychotic psychopathology (PwPP) (<em>n</em> = 63) compared with healthy control participants (<em>n</em> = 34) and biological relatives of PwPP (<em>n</em> = 44). Participants with schizophrenia (<em>n</em><span> = 31) showed impaired task performance compared with participants with bipolar disorder (</span><em>n</em><span><span> = 18). fMRI showed higher responses in the lateral occipital cortex of PwPP than in control participants. Using task-based </span>functional connectivity analyses, we observed abnormal connectivity between visual brain areas during contour perception among PwPP. These connectivity differences only emerged when participants had to distinguish the contour object from background distractors, suggesting that a failure to suppress noise elements relative to contour elements may underlie impaired contour processing in PwPP.</span></div></div><div><h3>Conclusions</h3><div>Our results are consistent with impaired contour integration in psychotic psychopathology, and especially schizophrenia, that is related to cognitive dysfunction<span> and may be linked to impaired functional connectivity across visual regions.</span></div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 2","pages":"Pages 229-241"},"PeriodicalIF":4.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142857002","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}
Pub Date : 2026-02-01DOI: 10.1016/S2451-9022(26)00010-8
{"title":"Guide for Authors","authors":"","doi":"10.1016/S2451-9022(26)00010-8","DOIUrl":"10.1016/S2451-9022(26)00010-8","url":null,"abstract":"","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 2","pages":"Pages A5-A11"},"PeriodicalIF":4.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146116533","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}
Pub Date : 2026-02-01DOI: 10.1016/j.bpsc.2025.09.013
Tobias Granwald , Federico Triolo , Máté Lengyel , Peter Dayan , Marc Guitart-Masip
Background
Learned helplessness has been suggested as a mechanism through which anhedonia in depression is developed. It has been theorized that this stems from a generalized pessimistic prior belief about the probability of success when attempting to actively avoid negative outcomes, thereby resulting in apathy and reduced motivation. However, how such a prior belief may relate to depression and apathy is unknown. Here, we leveraged a novel method based on cognitive tasks and Bayesian modeling to extract a reliable generalized prior belief expressing the probability with which negative outcomes are expected to be actively avoidable.
Methods
We quantified this prior belief in 521 nonclinical participants. Then we used Bayesian network analysis to explore how the prior’s mean was related to total scores of the Patient Health Questionnaire-9 (PHQ-9) depression scale, specific items of the PHQ-9, and 6 subscales measuring apathy, motivation, anhedonia, and emotional reactivity.
Results
We found that the mean of the prior belief was positively related to the tendency to get motivated to initiate and maintain goal-directed actions as measured with the Apathy Motivation Index (AMI) and not hedonic capacity as measured by the Snaith-Hamilton Pleasure Scale. Moreover, the same reverse-coded behavioral apathy subscale in the AMI was related to the total score of the PHQ-9 independently of hedonic capacity. Finally, the prior belief itself was not directly linked to depressive symptoms or PHQ-9 total scores.
Conclusions
These results indicate that our behavioral measure of helplessness is indirectly related to depressive symptoms through behavioral activation and independently of hedonic capacity.
{"title":"Exploring the Link Between a Prior Belief for Active Avoidance and Apathy, Anhedonia, and Depression: A Network Analysis","authors":"Tobias Granwald , Federico Triolo , Máté Lengyel , Peter Dayan , Marc Guitart-Masip","doi":"10.1016/j.bpsc.2025.09.013","DOIUrl":"10.1016/j.bpsc.2025.09.013","url":null,"abstract":"<div><h3>Background</h3><div>Learned helplessness has been suggested as a mechanism through which anhedonia in depression is developed. It has been theorized that this stems from a generalized pessimistic prior belief about the probability of success when attempting to actively avoid negative outcomes, thereby resulting in apathy and reduced motivation. However, how such a prior belief may relate to depression and apathy is unknown. Here, we leveraged a novel method based on cognitive tasks and Bayesian modeling to extract a reliable generalized prior belief expressing the probability with which negative outcomes are expected to be actively avoidable.</div></div><div><h3>Methods</h3><div>We quantified this prior belief in 521 nonclinical participants. Then we used Bayesian network analysis to explore how the prior’s mean was related to total scores of the Patient Health Questionnaire-9 (PHQ-9) depression scale, specific items of the PHQ-9, and 6 subscales measuring apathy, motivation, anhedonia, and emotional reactivity.</div></div><div><h3>Results</h3><div>We found that the mean of the prior belief was positively related to the tendency to get motivated to initiate and maintain goal-directed actions as measured with the Apathy Motivation Index (AMI) and not hedonic capacity as measured by the Snaith-Hamilton Pleasure Scale. Moreover, the same reverse-coded behavioral apathy subscale in the AMI was related to the total score of the PHQ-9 independently of hedonic capacity. Finally, the prior belief itself was not directly linked to depressive symptoms or PHQ-9 total scores.</div></div><div><h3>Conclusions</h3><div>These results indicate that our behavioral measure of helplessness is indirectly related to depressive symptoms through behavioral activation and independently of hedonic capacity.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 2","pages":"Pages 221-228"},"PeriodicalIF":4.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145126401","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}
Pub Date : 2026-01-01DOI: 10.1016/j.bpsc.2025.07.013
Sean A. Yarrell , Sophia H. Blyth , Alexandra B. Moussa-Tooks , Baxter P. Rogers , Anna Huang , Neil D. Woodward , Stephan Heckers , Roscoe O. Brady , Heather Burrell Ward
Background
Negative symptom severity predicts functional outcomes and quality of life in people with psychosis. However, negative symptoms respond poorly to medication, and existing literature has not converged on their neurobiological basis. Previous work in small schizophrenia samples has observed that lower cerebellar–dorsolateral prefrontal cortex (DLPFC) connectivity is associated with higher negative symptom severity and that increasing cerebellar-DLPFC connectivity with neuromodulation reduces negative symptoms. We extended this finding by testing associations between cerebellar-DLPFC connectivity, negative symptoms, and cognitive performance in a large sample of individuals with psychosis.
Methods
Individuals with psychosis spectrum disorders (N = 260) underwent resting-state functional magnetic resonance imaging and clinical characterization using the Positive and Negative Syndrome Scale and the Screen for Cognitive Impairment in Psychiatry. Using a previously identified cerebellar region as a seed, we measured connectivity to the DLPFC and regressed connectivity against negative symptom severity, covarying for age, sex, and scanner. Then, we tested whether cognitive performance indirectly affected the relationship between connectivity and negative symptom severity.
Results
Across the psychosis spectrum, higher cerebellar-DLPFC connectivity was associated with lower negative symptom severity (r = −0.17, p = .007). This connectivity–negative symptom relationship was not affected by psychosis subtype or duration of illness. Better delayed verbal learning was associated with higher cerebellar-DLPFC connectivity (r = 0.13, p = .034) and had a significant indirect effect on the relationship between connectivity and negative symptoms.
Conclusions
Our results extend relationships between cerebellar-DLPFC connectivity, negative symptom severity, and cognitive performance across the psychosis spectrum. Larger neuromodulation studies should test whether increasing cerebellar-DLPFC connectivity reduces negative symptoms in psychotic disorders.
{"title":"Cerebellar-Prefrontal Connectivity Predicts Negative Symptom Severity Across the Psychosis Spectrum","authors":"Sean A. Yarrell , Sophia H. Blyth , Alexandra B. Moussa-Tooks , Baxter P. Rogers , Anna Huang , Neil D. Woodward , Stephan Heckers , Roscoe O. Brady , Heather Burrell Ward","doi":"10.1016/j.bpsc.2025.07.013","DOIUrl":"10.1016/j.bpsc.2025.07.013","url":null,"abstract":"<div><h3>Background</h3><div>Negative symptom severity predicts functional outcomes and quality of life in people with psychosis. However, negative symptoms respond poorly to medication, and existing literature has not converged on their neurobiological basis. Previous work in small schizophrenia samples has observed that lower cerebellar–dorsolateral prefrontal cortex (DLPFC) connectivity is associated with higher negative symptom severity and that increasing cerebellar-DLPFC connectivity with neuromodulation reduces negative symptoms. We extended this finding by testing associations between cerebellar-DLPFC connectivity, negative symptoms, and cognitive performance in a large sample of individuals with psychosis.</div></div><div><h3>Methods</h3><div>Individuals with psychosis spectrum disorders (<em>N</em> = 260) underwent resting-state functional magnetic resonance imaging and clinical characterization using the Positive and Negative Syndrome Scale and the Screen for Cognitive Impairment in Psychiatry. Using a previously identified cerebellar region as a seed, we measured connectivity to the DLPFC and regressed connectivity against negative symptom severity, covarying for age, sex, and scanner. Then, we tested whether cognitive performance indirectly affected the relationship between connectivity and negative symptom severity.</div></div><div><h3>Results</h3><div>Across the psychosis spectrum, higher cerebellar-DLPFC connectivity was associated with lower negative symptom severity (<em>r</em> = −0.17, <em>p</em> = .007). This connectivity–negative symptom relationship was not affected by psychosis subtype or duration of illness. Better delayed verbal learning was associated with higher cerebellar-DLPFC connectivity (<em>r</em> = 0.13, <em>p</em> = .034) and had a significant indirect effect on the relationship between connectivity and negative symptoms.</div></div><div><h3>Conclusions</h3><div>Our results extend relationships between cerebellar-DLPFC connectivity, negative symptom severity, and cognitive performance across the psychosis spectrum. Larger neuromodulation studies should test whether increasing cerebellar-DLPFC connectivity reduces negative symptoms in psychotic disorders.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 1","pages":"Pages 116-125"},"PeriodicalIF":4.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859984","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}
Pub Date : 2026-01-01DOI: 10.1016/j.bpsc.2024.07.004
Prathik Kalva , Kourtney Kanja , Brian A. Metzger , Xiaoxu Fan , Brian Cui , Bailey Pascuzzi , John Magnotti , Madaline Mocchi , Raissa Mathura , Kelly R. Bijanki
To mitigate limitations of self-reported mood assessments, we introduce a novel affective bias task. The task quantifies instantaneous emotional state by leveraging the phenomenon of affective bias, in which people interpret external emotional stimuli in a manner consistent with their current emotional state. This study establishes task stability in measuring and tracking depressive symptoms in clinical and nonclinical populations. Initial assessment in a large nonclinical sample established normative ratings. Depressive symptoms were measured and compared with task performance in a nonclinical sample, as well as in a clinical cohort of individuals who were undergoing surgical evaluation for severe epilepsy. In both cohorts, a stronger negative affective bias was associated with a higher Beck Depression Inventory-II score. The affective bias task exhibited high stability and interrater reliability as well as construct validity in predicting depression levels in both cohorts, suggesting that the task is a reliable proxy for mood and a diagnostic tool for detecting depressive symptoms.
{"title":"Psychometric Properties of a Novel Affective Bias Task and Its Application in Clinical and Nonclinical Populations","authors":"Prathik Kalva , Kourtney Kanja , Brian A. Metzger , Xiaoxu Fan , Brian Cui , Bailey Pascuzzi , John Magnotti , Madaline Mocchi , Raissa Mathura , Kelly R. Bijanki","doi":"10.1016/j.bpsc.2024.07.004","DOIUrl":"10.1016/j.bpsc.2024.07.004","url":null,"abstract":"<div><div>To mitigate limitations of self-reported mood assessments, we introduce a novel affective bias task. The task quantifies instantaneous emotional state by leveraging the phenomenon of affective bias, in which people interpret external emotional stimuli in a manner consistent with their current emotional state. This study establishes task stability in measuring and tracking depressive symptoms in clinical and nonclinical populations. Initial assessment in a large nonclinical sample established normative ratings. Depressive symptoms were measured and compared with task performance in a nonclinical sample, as well as in a clinical cohort of individuals who were undergoing surgical evaluation for severe epilepsy. In both cohorts, a stronger negative affective bias was associated with a higher Beck Depression Inventory-II score. The affective bias task exhibited high stability and interrater reliability as well as construct validity in predicting depression levels in both cohorts, suggesting that the task is a reliable proxy for mood and a diagnostic tool for detecting depressive symptoms.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 1","pages":"Pages 126-131"},"PeriodicalIF":4.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735982","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}
Pub Date : 2026-01-01DOI: 10.1016/j.bpsc.2025.08.016
Jamie Roeske , Xiangyu Long , Meaghan V. Perdue , Madison Long , Bryce Geeraert , Mohammad Ghasoub , Keith Owen Yeates , Carly A. McMorris , Jacqueline Pei , W. Ben Gibbard , Christina Tortorelli , Catherine Lebel
Background
Prenatal alcohol exposure (PAE) has widespread effects on brain development. Alterations to the maturational timing of the amygdala, prefrontal cortex (PFC), and the white matter tracts connecting them may underlie behavioral differences, such as elevated risk taking and impulsivity in youth with PAE.
Methods
Here, we used T1 and diffusion-weighted magnetic resonance imaging to evaluate amygdala and PFC macrostructure (volume) and uncinate fasciculus and amygdala-PFC white matter tract microstructure (fractional anisotropy, mean diffusivity) development longitudinally in children and adolescents with PAE (n = 92 individuals [165 scans], ages 2–18 years) and unexposed participants (n = 148 individuals [606 scans], ages 2–17 years). We used generalized additive mixed-effects models to examine age-related changes in volume, fractional anisotropy, and mean diffusivity.
Results
Children and adolescents with PAE showed no significant amygdala volume development across the age range, and, compared with their unexposed counterparts, had shorter and delayed PFC development, earlier uncinate fasciculus development, and more protracted amygdala-PFC tract development in our age range. Participants with PAE also had smaller amygdala and PFC volumes, higher fractional anisotropy, and lower mean diffusivity in both tracts than unexposed individuals.
Conclusions
Our findings show altered maturational patterns in amygdala-PFC structures and circuitry among children and adolescents with PAE that suggest reduced brain plasticity. Differences in the developmental timing of these regions may underlie behavioral challenges, such as elevated risk taking and impulsivity, in those with PAE.
{"title":"Amygdala and Prefrontal Cortex Maturational Differences in Children and Adolescents With Prenatal Alcohol Exposure","authors":"Jamie Roeske , Xiangyu Long , Meaghan V. Perdue , Madison Long , Bryce Geeraert , Mohammad Ghasoub , Keith Owen Yeates , Carly A. McMorris , Jacqueline Pei , W. Ben Gibbard , Christina Tortorelli , Catherine Lebel","doi":"10.1016/j.bpsc.2025.08.016","DOIUrl":"10.1016/j.bpsc.2025.08.016","url":null,"abstract":"<div><h3>Background</h3><div>Prenatal alcohol exposure (PAE) has widespread effects on brain development. Alterations to the maturational timing of the amygdala, prefrontal cortex (PFC), and the white matter tracts connecting them may underlie behavioral differences, such as elevated risk taking and impulsivity in youth with PAE.</div></div><div><h3>Methods</h3><div>Here, we used T1 and diffusion-weighted magnetic resonance imaging to evaluate amygdala and PFC macrostructure (volume) and uncinate fasciculus and amygdala-PFC white matter tract microstructure (fractional anisotropy, mean diffusivity) development longitudinally in children and adolescents with PAE (<em>n</em> = 92 individuals [165 scans], ages 2–18 years) and unexposed participants (<em>n</em> = 148 individuals [606 scans], ages 2–17 years). We used generalized additive mixed-effects models to examine age-related changes in volume, fractional anisotropy, and mean diffusivity.</div></div><div><h3>Results</h3><div>Children and adolescents with PAE showed no significant amygdala volume development across the age range, and, compared with their unexposed counterparts, had shorter and delayed PFC development, earlier uncinate fasciculus development, and more protracted amygdala-PFC tract development in our age range. Participants with PAE also had smaller amygdala and PFC volumes, higher fractional anisotropy, and lower mean diffusivity in both tracts than unexposed individuals.</div></div><div><h3>Conclusions</h3><div>Our findings show altered maturational patterns in amygdala-PFC structures and circuitry among children and adolescents with PAE that suggest reduced brain plasticity. Differences in the developmental timing of these regions may underlie behavioral challenges, such as elevated risk taking and impulsivity, in those with PAE.</div></div>","PeriodicalId":54231,"journal":{"name":"Biological Psychiatry-Cognitive Neuroscience and Neuroimaging","volume":"11 1","pages":"Pages 17-29"},"PeriodicalIF":4.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145066730","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}
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