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Cognitive engagement in physical education is an important factor that reflects the quality of physical education teaching and influences students' learning outcomes. Effectively assessing students' cognitive engagement in physical education is valuable for classroom evaluation and instructional intervention. However, existing instruments for measuring cognitive engagement in physical education remain limited in contextual specificity, measurement accuracy, and practical applicability. Based on the ICAP framework, this study aimed to develop and validate the Cognitive Engagement in Physical Education Scale (CEPE) for Chinese middle school students. The scale was initially developed based on a literature review and classroom observations. A full reliability and validity test was conducted with 855 middle school students in Jinan, China. The final CEPE consisted of 14 items across four dimensions: observation and execution, cognitive processing, self-regulation, and collaborative innovation. The four-factor model showed acceptable fit to the data: χ2/ df = 4.396, RMSEA = 0.080, GFI = 0.919, CFI = 0.952, TLI = 0.938, IFI = 0.952, and SRMR = 0.041. Standardized factor loadings ranged from 0.68 to 0.97. The composite reliability values were all above 0.80, and the average variance extracted values were all above 0.50, supporting convergent validity. Although the Fornell-Larcker criterion was not fully satisfied for cognitive processing and self-regulation, additional evidence from HTMT values and competing model comparisons supported the discriminant validity of the four-factor structure. The CEPE total score and subscale scores were positively correlated with physical education learning self-efficacy, providing evidence of criterion-related validity. The CEPE developed in this study based on the ICAP framework showed acceptable reliability and validity. It may provide a useful measurement tool for assessing students' cognitive engagement in physical education.

Insulin signalling contributes to neurodevelopment and brain function, and insulin resistance (IR)-related traits are associated with cognitive performance. However, the genetic architecture shared across specific cognitive domains and IR-related phenotypes remains insufficiently defined. We analysed large-scale genome-wide association study summary statistics for 11 IR-related traits (N=53,334-933,970) and 10 cognitive measures (N=28,156-436,853) to quantify global and local genetic correlations, fine-map shared association signals, and annotate implicated genes and drug-gene interactions. Pairwise global and local genetic correlations were estimated, and shared high-confidence variants were prioritised using the multivariate Sum of Single Effects model. Positional and expression quantitative trait locus mapping was performed, and implicated genes were examined through functional annotation, tissue enrichment, and drug-gene interaction analyses. Low-to-moderate genetic correlations were observed between six IR-related traits and seven cognitive measures (|r g |=0.08-0.34), with predominantly opposite directions, except for correlations involving visual declarative short-term memory. Local genetic correlations showed mixed effect directions across most trait pairs, and multivariate fine-mapping prioritised 696 shared likely causal variants with high posterior support. Gene annotation indicated enrichment in several pathways, including immune-related, signal transduction, neurogenesis, neurotransmitter metabolism, receptor regulation, and lipid and cholesterol metabolism regulation. Implicated genes were expressed across various brain regions and showed prior associations with neuropsychiatric and cardiometabolic conditions. Several drug-gene interactions were identified, involving immunomodulatory and anti-inflammatory compounds. These findings indicate widespread heterogeneous genetic overlap between IR-related traits, particularly body mass index and waist-to-hip ratio, and cognitive measures of general intelligence, processing speed, and short-term visual declarative memory. The findings prioritise apolipoprotein-related lipid transport and inflammatory and oxidative stress pathways as candidate mechanisms linking cognitive, cardiometabolic, and neuropsychiatric phenotypes.

Accelerating urbanization has intensified psychological stress and mental health problems among urban residents. As accessible natural spaces for leisure and recreation, urban parks have received increasing scholarly attention for the potential restorative effects of their soundscapes. Existing studies have mainly focused on the restorative benefits of visual landscapes or examined only the direct relationship between soundscapes and perceived restorativeness. However, the potential psychological pathway through which soundscape cognitive image is associated with perceived restorativeness via emotional pleasure has not been sufficiently clarified. Based on the stimulus-organism-response framework, this study constructed a model linking soundscape cognitive image, emotional pleasure, and perceived restorativeness. Twelve urban parks in Foshan, China, were selected as case study sites. A field questionnaire survey was conducted among recreational visitors, and 300 valid responses were collected. Python 3.10 was used for data processing and descriptive analyses, and AMOS 26.0 was used for structural equation modeling and mediation tests. The results showed that soundscape cognitive image was positively associated with emotional pleasure. Soundscape cognitive image was positively associated with the being away, fascination, and compatibility dimensions of perceived restorativeness, whereas its direct relationship with coherence was not significant. Emotional pleasure was positively associated with being away and compatibility, was not significantly associated with fascination, and showed a significant negative association with coherence. Bootstrap analysis further indicated that emotional pleasure served as a significant indirect pathway between soundscape cognitive image and being away, compatibility, and coherence. The indirect pathway for coherence was negative and the total relationship was not significant, suggesting that this result should be interpreted cautiously. No significant indirect pathway was found for fascination. This study extends the application of the stimulus-organism-response framework to urban park soundscape research by showing how visitors' subjective soundscape cognition is related to perceived restorativeness through emotional pleasure. Because the study used cross-sectional self-report data, the findings should be interpreted as evidence of statistical associations and potential psychological pathways rather than as proof of causal effects. The results provide empirical references for soundscape evaluation and health-oriented urban park planning.

Sleep disturbances are associated with increased fatigue, reduced quality of life, and neurocognitive dysfunction and have emerged as a common complication among pediatric cancer survivors. Sleep disturbances are particularly concerning given their potential to exacerbate existing neurocognitive impacts of cancer treatments. This pilot study examined the feasibility and acceptability of a home-wearable EEG-based sleep device (Sleep ProfilerTM) for acute lymphoblastic leukemia (ALL) survivors as well as associations between specific sleep parameters and neurocognitive functioning. Children (ages 8-12; M = 10 years, SD = 1.6; N = 23) >6 months post-treatment for ALL were enrolled at clinical visits and wore the Sleep ProfilerTM for two consecutive nights at home, followed by neurocognitive testing of attention, inhibitory control, working memory, and processing speed. Parents completed subjective measures of child sleep, anxiety, depression, and acceptability. Feasibility reflected the percentage of children wearing the device at least one night and the percentage of nights with good EEG quality data. All participants wore the device both nights, with 84% meeting the threshold for good quality measurement. Few children met recommended quantity and quality sleep thresholds based on objective measurement, including 5 patients with elevated snoring levels; 43.5% of subjective ratings fell above the threshold for sleep disturbance. Greater sleep latency was associated with worse inhibitory control (r = -0.42, p = 0.046), and total sleep time was positively associated with inhibitory control and attention. Findings confirm the feasibility and acceptability of home EEG sleep monitoring in school-age survivors, and associations of sleep latency and snoring with reduced neurocognitive functioning may offer modifiable risk factors for aspects of neuropsychological dysfunction common in pediatric survivorship. At the time this study was conducted, we were not required to register the study on ClinicalTrials.gov. It was a single-institution feasibility study without intervention, which was not considered a clinical trial.

Resting-state network topology may provide a powerful framework for understanding how large-scale brain organisation supports cognitive functions. However, the topological correlates of social cognition remain poorly characterised. This study examined whether individual differences in social cognition are associated with the global topology of the resting-state functional connectome derived from high-density EEG across canonical frequency bands. Twenty-eight healthy young adults underwent a comprehensive neuropsychological assessment, including measures of global cognition, theory of mind, empathy, and social norm processing. High-density eyes-closed resting EEG was acquired, and source-reconstructed connectivity matrices were estimated using the phase-locking value. For each frequency band, global graph-theoretical measures of segregation (average clustering coefficient, CC), integration (characteristic path length, CPL), and small-worldness were computed. We found selective associations between network topology and the intrapersonal component of social norm processing. Higher intrapersonal norm scores were related to lower CC and longer CPL, predominantly in the theta and alpha bands. These relationships held after controlling for demographic variables and were supported by multivariate analyses. No other social cognition measures showed equally significant associations with resting-state EEG topology. These findings suggest that individual variability in intrapersonal social norm processing may be associated with differences in the global organisation of the intrinsic functional connectome and highlight the relevance of investigating normative aspects of social cognition within a resting-state connectomics framework.

The purpose of this study was to develop best practices for conducting cognitive debriefing interviews with pediatric populations by drawing on the currently available literature and insights from experts in the health-related quality of life research community. A scoping review of the literature was conducted to identify existing recommendations, considerations, and methods for conducting cognitive debriefing interviews with pediatric populations. Findings from the review informed the development of a draft set of best practices, which were subsequently reviewed and refined through a two‑round modified Delphi process. The Delphi panel was composed of experts (i.e., researchers) in patient-reported outcome instrument development and evaluation with experience conducting interviews with pediatric populations. Thirty-five articles or guidance documents were included in the final scoping review, contributing insights that were used to develop a draft set of 17 best practices. Following the two rounds of review by the Delphi panel, the final set of 17 best practices, which reflects panel consensus, addresses: developing the interview guide, evaluating the characteristics of the instrument to be debriefed, and interview conduct. The best practices described in this article provide evidence‑based guidance that can help to standardize and strengthen the rigor of cognitive debriefing interviews with pediatric populations while potentially also improving the experience for participants. Broader implementation across drug development programs may enhance the reliability of measurement, improve the quality of pediatric participant input, and promote more patient‑centered decision‑making.

Muscle synergies are traditionally viewed as stable, low-dimensional neuromuscular modules reflecting neural constraints. However, growing evidence suggests this mechanistic interpretation is incomplete. We propose a conceptual extension of the framework, arguing that coordination patterns reflected into multichannel EMG are emergent properties of an integrated cognitive-motor system rather than purely motor primitives. We identify three classes of non-motor factors that may shape motor output: (i) Task internalization and learning dynamics: synergy structure evolves with practice and the formation of internal models; (ii) affective and psychological states: emotional conditions (e.g., stress, anxiety) modulate muscle co-activation and stability; (iii) prior experience and sensorimotor memory: embodied history biases action selection and coordination. Consistent with predictive processing and embodied cognition, we argue these factors are constitutive dimensions of motor control rather than mere noise. This perspective implies that inter-subject variability in synergy structure reflects systematic differences in cognitive, affective, and experiential states. To enhance interpretability, we propose integrating minimal assessments into experimental designs: (i) task strategy evaluation, (ii) affective state characterization via physiological proxies or scales, (iii) documentation of prior motor experience, and (iv) analysis of learning trajectories. This integrative view complements existing models, providing a richer theoretical foundation to interpret variability, adaptability, and individual differences in human motor control.

This meta-analysis investigated the effects of functional magnetic resonance imaging neurofeedback (fMRI-NF) on inattention and cognitive dysfunctions. Using the keywords "fMRI neurofeedback" and "attention," randomized controlled trials were identified from major electronic databases from inception to June 2024. Outcomes were expressed as standardized mean differences (SMDs) with 95% confidence intervals (CIs). Five studies including 214 participants (mean age = 16.8 years) were analyzed. The median number of fMRI-NF sessions was four (range: 3-15), and the median follow-up duration was three weeks (range: 1-10 weeks). Stimulation sites included the right inferior frontal gyrus (n = 2), right anterior insular cortex (n = 1), dorsal anterior cingulate cortex (n = 1), and an individualized approach (n = 1). The primary analysis showed no significant difference in inattention improvement between the fMRI-NF and control groups (SMD = 0.17, 95% CI: -0.15 to 0.49, p = 0.30; four studies, 153 participants). Secondary outcomes also showed no significant intergroup differences, including vigilance (SMD = 0.08, 95% CI: -0.49 to 0.65, p = 0.79), inhibition (SMD = -0.68, 95% CI: -2.11 to 0.74, p = 0.35), and processing speed (SMD = -0.56, 95% CI: -1.38 to 0.27, p = 0.19). Heterogeneity was greater for the secondary outcomes than for the primary outcome, with I2 values of 49% for vigilance, 90% for inhibition, and 79% for processing speed, compared with 0% for the primary outcome. Given the limited evidence available to date, current evidence remains insufficient to draw robust conclusions regarding the therapeutic effectiveness of fMRI-NF.

Previous studies have revealed conflicting results as regards whether second language (L2) learners decompose morphologically complex words during online reading or process them in a whole-word manner. To resolve such controversies, first language (L1) morphological characteristics have been proposed as one factor leading to variation in L2 performance. Evidence for the argument of L1 morphological effects includes (1) that L2 learners from an L1 with a similar/congruent morphological feature outperform those from an L1 without a similar corresponding morphological feature and (2) that there is an advantage for L2 learners from an L1 with a more complex morphological system. In this paper, we examine the design of these studies and identify two potentially confounding factors that most studies have failed to consider when comparing L2 learners from different L1 morphological backgrounds: cognateness and L1 writing system. We suggest that studies examining L1 morphological effects recruit L2 groups whose L1s differ in their morphological system characteristics but share the same type of writing system, while also stringently excluding cognates in the design of experimental materials.

Accelerated biological aging can be assessed with DNA methylation (DNAm)-based epigenetic clocks. Research suggests that greater DNAm is associated with faster cognitive decline and risk of Alzheimer disease (AD) and other dementias. However, most studies have relied on single-time-point measurements of clocks, rather than evaluating dynamic changes over time. We examined the association between 15-year epigenetic aging trajectories and brain health outcomes in midlife. We analyzed 2,833 middle-aged adults (mean baseline age 40 years, 59% female and 44% Black) with &#x2265; 3 DunedinPACE (a recently developed epigenetic clock) measurements, collected over 15 years. Using mixed-effects modeling, we derived individual-specific slopes of epigenetic aging trajectories and categorized participants as Fast Agers (slopes > 1 SD above the mean), Slow Agers (slopes < 1 SD below the mean), or Typical Agers (within &#xb1;1 SD of the mean). We examined associations between trajectory group and cognition on five cognitive domains as well as on plasma AD biomarkers (NfL, p-tau217, A&#x3b2;42/A&#x3b2;40), all assessed 15-20 years post-baseline. Models were adjusted for demographics, education, physical activity and APOE *&#x3b5;4 carrier status (with additional adjustments for eGFRcr for biomarker outcomes). Epigenetic aging trajectories were associated with multiple domains of cognition and AD biomarkers (Figure 1). Compared to Typical Agers, Fast Agers showed worse processing speed, memory, executive function, and global cognition (all p<0.05), with no difference in verbal fluency. Slow Agers had better performance on memory and global cognition (both p < 0.05). Fast Agers also exhibited significantly lower A&#x3b2;42/A&#x3b2;40 levels (p = 0.011) compared to Typical agers; no significant associations with p-tau217 or NfL were observed in either group. Middle-aged adults with faster 15-year epigenetic aging trajectories demonstrated worse cognitive performance, whereas those with slower biological aging trajectories exhibited cognitive resilience and more favorable AD biomarker profiles. By examining long-term trajectories rather than single timepoints, these findings identify individuals at differential risk for brain health outcomes.

Persistent postural-perceptual dizziness (PPPD) is a chronic functional vestibular disorder characterized by persistent dizziness or postural instability that is exacerbated by upright posture, motion, and complex visual stimuli. Although neuroimaging studies suggest altered visual, vestibular, and emotional processing in PPPD, comprehensive resting-state functional magnetic resonance imaging evidence remains limited. This study investigated spontaneous brain activity and functional connectivity alterations in patients with PPPD. Twenty-one patients with PPPD and 23 healthy controls underwent 3.0 Tesla resting-state functional magnetic resonance imaging. Regional spontaneous brain activity and local synchronization were assessed using low-frequency fluctuation and regional homogeneity measures. Seed-based functional connectivity analyses were performed using the left insula, right anterior cingulate cortex, and left precuneus as seed regions. Between-group differences were tested with age and sex as covariates, and exploratory clinical-imaging correlation analyses were conducted in the patient group. Patients with PPPD showed altered spontaneous activity and local synchronization in the cerebellum, occipital and temporal cortices, frontal and parietal regions, anterior cingulate cortex, insula, precuneus, and motor-related areas. Functional connectivity analyses revealed abnormal connections among the insula, caudate nucleus, prefrontal cortex, supplementary motor area, anterior and posterior cingulate cortices, precuneus, fusiform gyrus, and superior temporal gyrus. Clinical-imaging correlation analyses further showed that disease duration, dizziness handicap, anxiety severity, and cognitive performance were associated with functional changes in visual, cerebellar, supplementary motor, superior parietal, cuneus, and precuneus regions. These findings indicate that PPPD involves distributed functional abnormalities in brain regions responsible for vestibular and postural integration, visual-spatial processing, emotional and salience monitoring, motor regulation, and self-referential cognitive processing. Abnormalities in these regions may contribute to persistent dizziness, postural instability, visual dependence, heightened symptom vigilance, anxiety-related symptom amplification, and insufficient postural-motor compensation. Thus, PPPD may be better understood as a distributed network disorder involving disrupted visual-vestibular-postural integration and maladaptive functional reorganization.

Posterior Cortical Atrophy (PCA) is a neurodegenerative syndrome defined by occipital atrophy that results in visuospatial deficits, often caused by Alzheimer's disease (AD) pathology. Patients with PCA are younger than typical AD patients and can present with anxiety. A rare and atypical variant of AD, the variable presentation of PCA has left it understudied, misdiagnosed, and with few in-depth examinations of cognitive profiles. This project reviews three patients referred for neuropsychological evaluation who were determined to have probable PCA. A comprehensive neuropsychological battery examined learning and memory, executive function, language, attention and processing speed, and visuospatial ability. Cases were examined based on cognitive complaints, daily functioning based on informant report, neuropsychological test performance, and neurodiagnostic work-up. Striking visuospatial deficits were observed in visuospatial construction tests (all patients scored&#x2009;<&#x2009;1 percentile), and performance was impaired on most tests with visual components. Memory scores were impaired on some tests, but scores were slightly better on a contextualized verbal task compared to a word list. Patients had trouble functioning related to vision (e.g. object finding, reading) and tested positive for AD biomarkers. These cases highlight key aspects of the neuropsychological work-up for suspected PCA, including visuospatial deficits, AD biomarkers, and cognitive complaints.

The human brain needs distributed, time-critical computation to efficiently solve complex problems. Turbulence provides such highly efficient spacetime information processing and transmission across widespread brain networks, yet we have been missing a mechanistic understanding of the interactions of turbulent vortices underlying human cognition. Here, we build the first whole-brain model of turbulent vortices as defined by the levels of local synchronization in brain signals quantifying turbulent interactions in vortex space. Specifically, using large-scale human neuroimaging data, we found that the interactions of turbulent vortices is an excellent framework for understanding cognition and brain computation. In particular, we show that when combined with connectome-based predictive modeling, this significantly predict the g-factor and the scores on the underlying tasks. In addition, turbulent vortices also distinguish the detailed spacetime dynamics of rest and cognition-and can even distinguish between subtle subcomponents of cognitive tasks, where manipulation of vortices can be shown to change cognition. Overall, this whole-brain framework creates a natural vortex space for the brain computation underlying cognition, as well as potentially providing novel ways of controlling turbulent interactions in disease. Turbulence allows for distributed, time-critical computation to efficiently solve complex problems using efficient spacetime information processing and transmission across widespread brain networks. This is the first whole-brain model of turbulent vortices defined by the levels of local synchronization in brain signals quantifying turbulent interactions in vortex space. In large-scale human neuroimaging data, used connectome-based predictive modeling to significantly predict behavior on tasks. In addition, turbulent vortices also distinguish the detailed spacetime dynamics of rest and cognition&#x2014;and can even distinguish between subtle subcomponents of cognitive tasks, where manipulation of vortices can be shown to change cognition. Overall, this whole-brain framework creates a natural vortex space for the brain computation underlying cognition, as well as potentially providing novel ways of controlling turbulent interactions in disease.

Understanding how brain networks operate across different frequencies during cognitive tasks, and how these dynamics change with age, remains a central challenge in cognitive neuroscience. While previous studies have focused on resting-state activity and passive listening, less is known about frequency-specific brain dynamics during event-related tasks that require active memory engagement. In this study, we extend the recently developed FREQ-NESS analytical pipeline by adapting it to event-related task and resting-state source-reconstructed magnetoencephalography (MEG) data from 140 healthy participants. This method quantified the variance explained by frequency-specific brain networks, their spatial organization, and associated time-resolved power estimates. We found significant effects of age, condition, and their interaction in the variance explained by leading components at 8.6, 10.0, and 20.0 Hz. Older adults exhibited peaks at 8.6 and 10.0 Hz across both rest and task, while younger adults displayed a task-related reduction, suggesting a different organization of brain networks during memory processing with age. Time-frequency analysis revealed age- and condition-dependent desynchronization in the alpha and beta bands (7.1-22.9 Hz). These findings demonstrate the effectiveness of the adapted FREQ-NESS pipeline for event-related tasks and highlight the importance of frequency-resolved network analysis for characterizing age-related changes in active auditory memory processing.

Hearing loss is associated with accelerated cognitive decline, and auditory rehabilitation via cochlear implantation (CI) may mitigate this trajectory. In the past, the impact of cochlear implantation on different cognitive subdomains has been described. However, verbal fluency (VF), which requires fast semantic retrieval, executive control, and processing speed, and is predictive of dementia risk and overall survival, has been rarely studied and control groups are mostly missing due to ethical reasons. The present study compares long-term VF trajectories in CI recipients and untreated hearing-impaired controls from a large population-based aging study. VF was assessed in 74 CI recipients (M&#x202f;=&#x202f;65.6&#x202f;years, SD&#x202f;=&#x202f;9.1) at pre-operative baseline and 1, 2, 4.5, and up to 9&#x202f;years post-implantation, and in 383 untreated hearing-impaired participants (M&#x202f;=&#x202f;72.6&#x202f;years, SD&#x202f;=&#x202f;10.0) from the English Longitudinal Study of Ageing (ELSA) across a comparable time frame. Scores were z-standardized within each study to enable cross-cohort comparison. Linear mixed-effects models were used to compare VF trajectories, with age, sex, and education as covariates. VF trajectories differed significantly between groups (Time&#x202f;&#xd7;&#x202f;Study interaction: b&#x202f;=&#x202f;0.562, p&#x202f;<&#x202f;0.001). The ELSA cohort showed a steady linear decline over time (b&#x202f;=&#x202f;-0.261, p&#x202f;=&#x202f;0.001), whereas the CI cohort exhibited an inverted-U trajectory with initial improvement followed by a plateau. After propensity score matching, results remained robust. Cochlear implantation is associated with more favorable long-term verbal fluency trajectories compared to untreated hearing loss. These findings add to the growing evidence that auditory rehabilitation may help preserve cognitive function in older adults.

Mature brain-derived neurotrophic factor has long been known to as an epigenetic regulator. It is excessively secreted after status epilepticus, leading to a variety of permanent structural and functional changes in the brain. While its precursor forms proBDNF regulates nerve development, neural transmission and cognitive function, it is not fully known whether the expression of proBDNF is changed in vivo or how it influences neuronal signaling and function ultimately leading to spatial cognitive impairments. Here, we investigated changes in proBDNF levels in the hippocampus of the pentylenetetrazole (pentylenetetrazole)-induced epileptic rat model. Functional blocking of proBDNF singling and its related pathway in the hippocampal regions was conducted to explore the potential mechanisms. Meanwhile, local field potentials were recorded in the hippocampal CA3-CA1 pathway and the directionality of neural information flow (NIF) between two regions was evaluated. We found that seizures were induced by PTZ-treated rats, which exhibited excessive proBDNF expression in the hippocampus only after undergoing behavioral training. Intra-hippocampal infusions of anti-proBDNF antibody into the CA1 but not the CA3 region could mitigate the PTZ-induced memory consolidation deficits and we confirmed the involvement of p75NTR rather than TrkB signaling. The excessive proBDNF could act on both presynaptic and postsynaptic sites through p75NTR signaling to exaggerate neural activity of putative fast-spiking interneurons. This was evidenced by increased spontaneous excitatory postsynaptic current frequency and amplitude, and further corroborated by action potential-independent miniature EPSC (mEPSC) recordings, which revealed concurrent increases in both mEPSC frequency and amplitude specifically in the epilepsy group. Importantly, this over-expression of proBDNF disrupted phase synchronization and directional coupling strength at the CA3 to CA1 synapses. However, blocking proBDNF or inactivation of the p75NTR signaling could effectively enhance the phase-locked value and neural information flow at the gamma and high-frequency oscillations, and significantly alleviate the PTZ-induced impairments in memory processing. Our findings are consistent with the hypothesis and provide the first direct evidence that the over-activation of proBDNF signaling represents a potential mechanism involved in neural dysfunction and NIF disruption leading to memory impairments in kindled animals.

Adolescent externalizing behavior is a major risk factor for later substance use and other psychiatric outcomes. Understanding its genetic architecture and its relationships with brain imaging phenotypes requires scalable genome-wide methods that can be applied to youth cohorts. Using data from the Adolescent Brain Cognitive Development (ABCD) Study &#xae; , we implemented a pipeline for conducting genome-wide association studies (GWAS) of longitudinal externalizing traits and multimodal imaging-derived phenotypes (IDPs). We performed quality-controlled genotype processing and constructed harmonized phenotype and covariate datasets. GWAS analyses were conducted using REGENIE in a two-step framework. In Step 1, ridge regression prediction models were trained using linkage disequilibrium (LD)-pruned variants. In Step 2, genome-wide association testing was performed for each phenotype. The analyses included three externalizing phenotypes-baseline, longitudinal mean, and longitudinal slope-and approximately 200 IDPs measured at baseline or summarized using their longitudinal means and slopes. We additionally constructed a custom LD reference panel using unrelated individuals and calculated LD scores using LD Score Regression software (LDSC). Genome-wide genetic correlations between externalizing traits and imaging phenotypes were subsequently estimated using cross-trait LD Score Regression. This exploratory study systematically evaluated genome-wide genetic correlations between regional cortical morphology and externalizing phenotypes during adolescence. Although several associations reached nominal statistical significance, none remained significant after correction for multiple comparisons. These results should not be interpreted as evidence for the absence of shared genetic architecture. Instead, the precision of the genetic-correlation estimates was limited by the available imaging GWAS sample size, uncertainty in SNP-based heritability estimates, and the large number of regional comparisons. Larger imaging-genetics samples and independent replication studies will be required to determine whether modest or regionally specific genetic correlations exist.

Despite many years of research, the quest to identify neural correlates of perceptual consciousness (NCC) remains unresolved. One major obstacle lies in methodological limitations: most studies rely on non-invasive neural measures with limited spatial or temporal resolution, making it difficult to disentangle proper NCCs from concurrent cognitive processes. Additionally, the relatively low sensitivity of non-invasive neural measures limits the interpretation of null findings in studies targeting proper NCCs. In this review, we discuss how human intracranial recordings can advance the search for NCCs by offering high spatiotemporal resolution, improved signal sensitivity, and broad cortical and subcortical coverage. We review studies that have examined NCCs at the level of single neurons and populations of neurons, and evaluate their implications on the debates between cognitive and sensory theories of consciousness. Finally, we highlight the limits of current intracranial human recordings and propose future directions based on emerging technologies and novel experimental paradigms.

Glucagon-like peptide-1 receptor (GLP1R) is a G-protein-coupled receptor recognized for its essential role in metabolic homeostasis and insulin secretion. Emerging evidence suggests that central GLP-1 signaling also modulates sensory information processing and cognitive functions. The thalamic reticular nucleus (TRN) serves as a critical inhibitory hub that filters and prioritizes sensory transmission between the thalamus and the cerebral cortex. We have identified a distinct population of GLP1R-expressing neurons distributed within the TRN; however, their long-range structural connectivity remains largely uncharacterized. In this study we used Glp1r-Cre mice combined with viral-genetic tracing strategies to map the whole-brain inputs and outputs of GLP1R-linked neurons. To identify direct monosynaptic inputs, a Cre-dependent retrograde rabies virus system was employed. To delineate the efferent axonal projections, a Cre-dependent synaptophysin-based tracing strategy was employed. GLP1R neurons exhibited a distinct rostrocaudal distribution, with most located in the middle region of the TRN. The starter neurons, identified by the colocalization of adeno-associated virus (AAV)-double-floxed inverted orientation (DIO)-enhanced green fluorescent protein (EGFP)-tumor virus A receptor (TVA), AAV-DIO-rabies virus glycoprotein from the CVS-N2c strain (N2cG), and rabies virus (RV)-envelope protein A (EnvA)-glycoprotein-deleted (&#x394;G)-mCherry, were primarily located in the TRN. Retrograde-labeled neurons were identified across numerous brain regions. Dense clusters of input neurons were observed in the primary and secondary motor cortices (M1 and M2, respectively) and the primary somatosensory cortex (S1). Substantial inputs were observed, including from the ventrolateral (VL), central lateral (CL), and posterior (Po) thalamic nuclei. Additionally, notable presynaptic labeling was detected in subcortical regions such as the zona incerta (ZI) and lateral hypothalamic area (LH), as well as midbrain structures including the substantia nigra pars reticulata (SNR) and the deep mesencephalic nucleus (DpMe). Anterograde synaptophysin-based mapping revealed that TRNGLP1R neurons selectively project to the ventral medial nucleus (VM), paracentral thalamic nucleus (PC), mediodorsal thalamus, lateral part (MDL), and lateral habenula (LHb) nuclei. The results confirm the existence of complex long-range afferent and efferent circuits associated with TRNGLP1R neurons, providing a morphological basis for studying their role in integrating metabolic states with sensory gating.