Frontiers in Behavioral Neuroscience最新文献

{"title":"Structurally restricted message-passing within shallow architectures for explainable network-level brain decoding on small cohorts.","authors":"José Diogo Marques Dos Santos, Maria Beatriz Ramos, Luís Paulo Reis, José Paulo Marques Dos Santos, Bruno Direito","doi":"10.3389/fnbeh.2026.1833995","DOIUrl":"10.3389/fnbeh.2026.1833995","url":null,"abstract":"<p><strong>Introduction: </strong>Applying artificial intelligence to functional magnetic resonance imaging (fMRI) has advanced the modelling of neural activity, but deep architectures such as graph neural networks (GNNs) require large samples, limiting their use in the small cohorts typical of task-based fMRI. Shallow neural networks (SNNs) are robust with few samples but treat brain regions independently, overlooking the brain's network organization. We propose a structurally constrained message-passing framework that integrates diffusion-based structural connectivity, from a previously published group connectome, with region-level fMRI signals in a shallow architecture.</p><p><strong>Methods: </strong>The task is a binary classification of individual video trials as mentalizing or random, decoded from the fMRI response, in a Theory of Mind paradigm from the Human Connectome Project Young Adult dataset (30 subjects) under subject-wise 3-fold cross-validation. Two shallow classifiers are compared on the same data: the baseline classifies each trial from the regional fMRI signals as independent inputs, whereas the proposed model first applies one message-passing step, replacing each region's signal with a structurally connected combination of its neighbors' signals, so that classification operates at the level of anatomically defined networks. Interpretability is assessed using SHAP (SHapley Additive exPlanations).</p><p><strong>Results: </strong>Across folds, the proposed model matches the baseline (mean retrained accuracy 85.1%; 84.7% on the shared partition), the accuracy lost to pruning being recovered by retraining in every fold. The magnitude of the inputs' contributions is reproducible across folds, whereas their direction is not. Only about a quarter of the consistently retained inputs also preserve their sign, so a cross-fold sign-consistency criterion is applied to retain reliable explanations. This identifies seven networks contributing robustly to the mentalizing class, located in the temporo-parietal junction, inferior parietal, and medial temporal cortices and overlapping a literature-based mentalizing map (overlap coefficient 0.383). Within these networks, Cohen's D ranks the relative signal magnitude of the constituent regions.</p><p><strong>Discussion: </strong>Overall, structural constraints improve biological interpretability without compromising classification performance, while cross-validation establishes which explanations are stable, offering a compact and interpretable approach to network-level brain decoding in small cohorts and a basis that may be applied to connectivity disorders.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1833995"},"PeriodicalIF":3.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Essential element and toxic metal dyshomeostasis in childhood autism spectrum disorder: a comprehensive narrative review of correlations, tissue-specific distribution, and multifactorial regulation.","authors":"Qian Du, Qunying Zhou, Li Yu, Yunchao Ye, Xiaoling Wu","doi":"10.3389/fnbeh.2026.1944510","DOIUrl":"10.3389/fnbeh.2026.1944510","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social communication and repetitive stereotyped behaviors, with a rising global prevalence. Its etiology involves genetic, environmental, and epigenetic interactions, among which essential elements [including trace elements such as zinc (Zn), selenium (Se), copper (Cu), iron (Fe), manganese (Mn) and macrominerals like magnesium (Mg)] and toxic metals (lead (Pb), mercury (Hg), cadmium (Cd)) are key environmental regulators of neurodevelopment. This narrative review systematically summarizes the association between these elements and ASD in children. Core findings confirm that Zn/Se/Fe/Mg deficiency, tissue-specific Cu imbalance (elevated plasma, reduced hair), Pb/Hg accumulation, and Zn-Cu ratio imbalance are significantly correlated with ASD occurrence and severity. These abnormalities disrupt neurotransmitter homeostasis, oxidative stress balance, and synaptic plasticity, which pathways closely linked to ASD pathogenesis. Critically, we highlight the tissue-specific distribution patterns of these elements (differences across blood, hair, urine, and nails) and the multifactorial regulatory network involving genetic variants (e.g., metal transporter genes, metallothioneins), environmental exposures (diet, pollutants, pesticides), individual differences (age, gender), and comorbidities (gastrointestinal dysfunction). Intervention evidence shows that supplementing deficient essential elements or reducing toxic metal exposure may alleviate ASD symptoms, though study quality and methodological heterogeneity limit causal inferences. This review provides a theoretical basis for ASD pathogenesis research, early diagnosis, and targeted element-based interventions.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1944510"},"PeriodicalIF":3.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of challenging exercise in improving behavioral dysfunction in a mouse model of Parkinson's disease.","authors":"Yuan Zeng, Ping Chen, Quan Yang, Bing Liu, Liuting Huang, Kai Zhang, Shumin Liu","doi":"10.3389/fnbeh.2026.1887753","DOIUrl":"https://doi.org/10.3389/fnbeh.2026.1887753","url":null,"abstract":"<p><strong>Objective: </strong>To investigate whether accelerated rotarod exercise preconditioning provides greater neuroprotection than constant-speed training in a 6-OHDA mouse model of Parkinson's disease (PD).</p><p><strong>Methods: </strong>Male C57BL/6 mice were assigned to four groups: sham-operated sedentary (Con), PD sedentary (PD), constant-speed exercise + PD (Gen+PD, 10 rpm), and accelerated exercise + PD (Acc+PD, 5-40 rpm). Both exercise groups completed 4 weeks of rotarod training (240 s/session, 6 sessions/day, 5 days/week) before unilateral intrastriatal 6-OHDA injection. Con mice received vehicle at identical coordinates. Motor function was assessed by APO-induced rotation, negative geotaxis, pole, and open field tests. Striatal dopamine (DA) was quantified by ELISA; BDNF, TrkB, and TH expression were measured at the mRNA (RT-qPCR) and protein (Western blot) levels in the striatum and substantia nigra.</p><p><strong>Results: </strong>Relative to the PD group, Acc+PD mice showed significant reductions in negative geotaxis turning latency, T-turn, and T-total (all <i>P</i> < 0.01), and significant increases in total locomotor distance, mean speed, and central zone dwell time (all <i>P</i> < 0.01). Striatal DA content was markedly elevated in the Acc+PD group (<i>P</i> < 0.01). BDNF and TrkB mRNA were significantly upregulated in both the striatum and substantia nigra (<i>P</i> < 0.01), and TH, BDNF, and TrkB protein levels in the substantia nigra were substantially increased (<i>P</i> < 0.01). Improvements in the Gen+PD group were more modest and restricted in scope. Across all indices, the Acc+PD group consistently outperformed the Gen+PD group.</p><p><strong>Conclusion: </strong>Four weeks of acceleration-based rotarod preconditioning substantially delayed behavioral deficits in 6-OHDA-lesioned mice, accompanied by greater preservation of striatal DA and broader upregulation of TH, BDNF, and TrkB compared with constant-speed training. These findings identify exercise intensity as a critical determinant of preconditioning efficacy and support accelerated rotarod training as a more effective neuroprotective strategy in this PD model.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1887753"},"PeriodicalIF":3.4,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13627359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Childhood trauma and psychological symptoms in young adults: examining the mediating role of vulnerable narcissism and the moderating role of psychological resilience.","authors":"Fatih Cebeci","doi":"10.3389/fnbeh.2026.1904564","DOIUrl":"https://doi.org/10.3389/fnbeh.2026.1904564","url":null,"abstract":"<p><strong>Introduction: </strong>Childhood trauma is consistently associated with symptoms of depression, anxiety, and stress, yet the self-related processes and adaptive resources relevant to these associations remain insufficiently understood. This study examined whether vulnerable narcissism statistically mediated the associations between childhood trauma and these three symptom domains and whether psychological resilience moderated the associations between vulnerable narcissism and these symptoms.</p><p><strong>Methods: </strong>A cross-sectional convenience sample of 571 young adults aged 18-30 years was recruited online from Türkiye. Of the participants, 76.7% were women, and the sample largely comprised individuals engaged in university education. Participants completed the Childhood Trauma Questionnaire-33, the eight-item Vulnerable Narcissism Scale, the Brief Resilience Scale, and the Depression Anxiety Stress Scales-21. Regression-based mediation and moderated mediation analyses were conducted using 5,000 bootstrap samples and heteroscedasticity-consistent standard errors.</p><p><strong>Results: </strong>Childhood trauma and vulnerable narcissism were positively associated with depression, anxiety, and stress symptoms, whereas psychological resilience was negatively associated with all three symptom domains. The indirect associations between childhood trauma and depression, anxiety, and stress through vulnerable narcissism were statistically significant, while the corresponding direct associations remained significant. However, psychological resilience did not moderate the associations between vulnerable narcissism and any of the three symptom domains or the indirect associations through vulnerable narcissism.</p><p><strong>Discussion: </strong>The findings support partial statistical mediation through vulnerable narcissism within the specified model but do not establish a temporal, developmental, or causal sequence. Psychological resilience was independently associated with lower symptom levels but did not function as a moderator in the proposed model.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1904564"},"PeriodicalIF":3.4,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The medial prefrontal cortex is required for prospective navigation in spatial sequential memory.","authors":"Jihyun Lee, Eunsol Cho, Yong Sang Jo","doi":"10.3389/fnbeh.2026.1930201","DOIUrl":"10.3389/fnbeh.2026.1930201","url":null,"abstract":"<p><p>Goal-directed spatial navigation depends not only on the retrieval of past experiences but also on the prospective representation of future paths. The medial prefrontal cortex (mPFC) is well-established as a critical region for executive functions, particularly in supporting goal-directed behavior and prospective information processing. Although recent electrophysiological recordings show that mPFC neuronal ensembles exhibit predictive codes for future movement directions, a clear behavioral demonstration of whether this region is causally required for prospective navigation remains to be determined. To address this question, we developed a novel spatial sequential memory task using a modified water maze, in which the escape platform moved along a circular path by a constant angle and direction across trials within each day. Using this paradigm, functional dissociation within the prefrontal cortex was investigated by targeting bilateral excitotoxic lesions to two distinct subregions: the mPFC and the anterior cingulate cortex (ACC). Our results demonstrated that mPFC lesions, but not ACC lesions, selectively disrupted the ability to predict and navigate toward the subsequent escape platform location. Furthermore, this behavioral deficit, characterized by disorganized search patterns, occurred without impairment of retrospective navigation to the previously visited location. These findings suggest that the mPFC is essential for prospective spatial navigation, integrating sequential rules with spatial information to generate future trajectories.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1930201"},"PeriodicalIF":3.4,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13619581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Impact of inhaled particulates and toxicants on brain health: inflammation mechanisms and behavioral consequences.","authors":"Racheal O Asaolu, Jagan Srinivasan, Benjamin C Nephew","doi":"10.3389/fnbeh.2026.1937586","DOIUrl":"https://doi.org/10.3389/fnbeh.2026.1937586","url":null,"abstract":"","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1937586"},"PeriodicalIF":3.4,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Median nerve electrical stimulation promotes myelin regeneration through regulating miR-1-3p/BDNF/TrkB-MAPK pathway in a transient cerebral ischemia rat model.","authors":"Rui Li, Jingyi Lu, Chengcai Zhang, Xiaowei Zhang, Meiqi Wang, Ping Zhang, Kunli Yang, Hongmei Fang, Ying Gao, Kistina Mohamed, Che Ismail Che Noh, Yi Li, Kai Ling Chin","doi":"10.3389/fnbeh.2026.1820913","DOIUrl":"10.3389/fnbeh.2026.1820913","url":null,"abstract":"<p><strong>Introduction: </strong>Median nerve electrical stimulation (MNES) has emerged as a promising peripheral neuromodulatory strategy for improving motor recovery after ischemic stroke. Because the median nerve provides strong afferent input to central sensorimotor pathways, MNES may influence post-stroke neural repair beyond symptomatic motor modulation. However, the molecular mechanisms linking MNES to myelin repair remain unclear. Brain-derived neurotrophic factor (BDNF) is closely involved in neuronal survival, plasticity, and myelin remodeling, and bioinformatic analysis identified BDNF as a putative target of miR-1-3p. Therefore, this study investigated whether MNES-associated neurological recovery and myelin repair after ischemic stroke involve modulation of the miR-1-3p/BDNF/TrkB-MAPK pathway.</p><p><strong>Methods: </strong>Adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R), followed by MNES every other day for seven sessions. Neurological function, infarct injury, neuronal survival, neuroinflammation, myelin integrity, and pathway-related molecular changes were evaluated using behavioral, histological, ultrastructural, RT-qPCR, and Western blot analyses.</p><p><strong>Results: </strong>MNES was associated with improved neurological performance, reduced infarct injury, better preservation of myelin structure, decreased miR-1-3p expression, and increased BDNF, TrkB, and MAPK expression. In miR-1-3p modulation experiments, miR-1-3p antagomir partially mimicked the neuroprotective and myelin-related effects observed after MNES, whereas miR-1-3p agomir attenuated several MNES-associated benefits and reduced BDNF/TrkB-MAPK pathway-related protein expression.</p><p><strong>Conclusion: </strong>These findings suggest that MNES may support early neurological recovery and myelin repair after ischemic stroke, at least in part through involvement of the miR-1-3p/BDNF/TrkB-MAPK pathway. Further studies are required to confirm direct molecular targeting, long-term efficacy, safety, and translational relevance.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1820913"},"PeriodicalIF":3.4,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13612498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of <i>Cola nitida</i> against dexamethasone- and scopolamine-induced cognitive and cardiac dysfunction.","authors":"Lawrence Dayo Adedayo, Olugbenga S Michael, Gideon Opeyemi Ayilara, Mayode Elizabeth Olumoroti, Olubayode Bamidele, Saminu Samaila, Ibtihel Dhaya, Nafisat Dasola Akorede, Patrick Oluwole Abolarin, Laurette N Ofodile","doi":"10.3389/fnbeh.2026.1803200","DOIUrl":"10.3389/fnbeh.2026.1803200","url":null,"abstract":"<p><strong>Background: </strong>Cognitive dysfunction and cardiometabolic disturbances frequently coexist in neurological and metabolic disorders. Chronic systemic inflammation in cardiometabolic syndrome may promote neuroinflammation, damaging neurons and synapses and impairing memory pathways. <i>Cola nitida</i> is a medicinal plant widely recognized for its stimulant and therapeutic properties, yet its neuroprotective and cardiometabolic effects remain underexplored. Objective: This study investigated the effects of methanol extract of <i>Cola nitida</i> (CN) in a mouse model of memory and metabolic dysfunction induced by scopolamine and dexamethasone.</p><p><strong>Methods: </strong>Male mice were randomly divided into six groups (<i>n</i> = 5): control (saline), scopolamine (3 mg/kg), scopolamine + dexamethasone (0.2 mg/kg), CN (50 mg/kg) + scopolamine, CN + scopolamine + dexamethasone, and donepezil (1 mg/kg) + scopolamine + dexamethasone. Treatments lasted 7 days, followed by behavioral testing (Morris Water Maze, Y-Maze). Biochemical analyses included acetylcholinesterase activity, oral glucose tolerance, lactate/LDH, oxidative stress markers, and lipid profiles. Hippocampal histology assessed neurodegeneration, while molecular docking evaluated CN phytochemicals against proteins linked to glucose metabolism, oxidative stress, and cholinergic signaling.</p><p><strong>Results: </strong>Co-administration of dexamethasone and scopolamine impaired memory, elevated AChE activity, fasting glucose, and oxidative stress in the brain and heart. CN treatment improved memory and glucose tolerance, reduced oxidative stress and AChE activity, and preserved hippocampal neuronal integrity. Docking revealed strong affinities of CN flavonoids and procyanidins for Akt, GLP-1 receptor, Keap1, AChE, and TYK2, implicating them in glucose regulation, redox balance, and cholinergic neurotransmission.</p><p><strong>Conclusion: </strong>These findings highlight the neuroprotective and cardiometabolic benefits of <i>Cola nitida</i> and support its therapeutic potential for cognitive and metabolic disorders.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1803200"},"PeriodicalIF":3.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13597722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Whole-brain cFos mapping reveals the paraventricular thalamus as a key node for stress-enhanced fear learning.","authors":"Michael R Martino, Jade Baek, Megan J Francis, Bayleigh Pagoota, Anna C Tsyrulnikov, Jacqueline E Paniccia, Rachel E Clarke, Logan M Manusky, Alexander C W Smith, James M Otis","doi":"10.3389/fnbeh.2026.1866792","DOIUrl":"10.3389/fnbeh.2026.1866792","url":null,"abstract":"<p><strong>Introduction: </strong>Fear learning is critical for organisms to respond appropriately to potentially harmful stimuli. In cases of post-traumatic stress disorder (PTSD), potent or persistent trauma can facilitate future aversive learning, leading to maladaptive fear responses in generally safe contexts. Despite this knowledge, the neural circuit mechanisms that underlie stress-enhanced fear learning (SEFL) remain poorly understood.</p><p><strong>Methods: </strong>We utilized brain clearing and light sheet imaging, mapping whole-brain expression of the immediate early gene cFos in mice to identify brain regions engaged by SEFL. Next, we used chemogenetics to test the causal contribution of a candidate target region, the paraventricular thalamus (PVT), to sensitized fear learning.</p><p><strong>Results: </strong>SEFL was associated with reduced activity throughout the brain, most prominently within higher order thalamic nuclei. Despite the overall reduction, cFos expression in the PVT positively correlated with a principal-component-derived predictor of subsequent sensitized fear expression. Furthermore, chemogenetic inhibition of the PVT 30 days after stress exposure prevented the acquisition of SEFL and restored freezing to control levels.</p><p><strong>Discussion: </strong>Our results provide a comprehensive whole-brain SEFL-induced cFos map. Furthermore, we reveal a novel function for one identified brain region, the PVT, in sensitized fear learning.</p>","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1866792"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Psychopathological and behavioral trajectories in transitional-age youth: innovative approaches and paradigms.","authors":"Michele Poletti, Gianluca Castelnuovo, Lorenzo Pelizza","doi":"10.3389/fnbeh.2026.1958484","DOIUrl":"https://doi.org/10.3389/fnbeh.2026.1958484","url":null,"abstract":"","PeriodicalId":12368,"journal":{"name":"Frontiers in Behavioral Neuroscience","volume":"20 ","pages":"1958484"},"PeriodicalIF":3.4,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13591151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}