Dynamic causal modeling analysis reveals the modulation of motor cortex and integration in superior temporal gyrus during multisensory speech perception.

The processing of speech information from various sensory modalities is crucial for human communication. Both left posterior superior temporal gyrus (pSTG) and motor cortex importantly involve in the multisensory speech perception. However, the dynamic integration of primary sensory regions to pSTG and the motor cortex remain unclear. Here, we implemented a behavioral experiment of classical McGurk effect paradigm and acquired the task functional magnetic resonance imaging (fMRI) data during synchronized audiovisual syllabic perception from 63 normal adults. We conducted dynamic causal modeling (DCM) analysis to explore the cross-modal interactions among the left pSTG, left precentral gyrus (PrG), left middle superior temporal gyrus (mSTG), and left fusiform gyrus (FuG). Bayesian model selection favored a winning model that included modulations of connections to PrG (mSTG → PrG, FuG → PrG), from PrG (PrG → mSTG, PrG → FuG), and to pSTG (mSTG → pSTG, FuG → pSTG). Moreover, the coupling strength of the above connections correlated with behavioral McGurk susceptibility. In addition, significant differences were found in the coupling strength of these connections between strong and weak McGurk perceivers. Strong perceivers modulated less inhibitory visual influence, allowed less excitatory auditory information flowing into PrG, but integrated more audiovisual information in pSTG. Taken together, our findings show that the PrG and pSTG interact dynamically with primary cortices during audiovisual speech, and support the motor cortex plays a specifically functional role in modulating the gain and salience between auditory and visual modalities. Supplementary Information: The online version contains supplementary material available at 10.1007/s11571-023-09945-z.

Atypical dynamic neural configuration in autism spectrum disorder and its relationship to gene expression profiles.

Although it is well recognized that autism spectrum disorder (ASD) is associated with atypical dynamic functional connectivity patterns, the dynamic changes in brain intrinsic activity over each time point and the potential molecular mechanisms associated with atypical dynamic temporal characteristics in ASD remain unclear. Here, we employed the Hidden Markov Model (HMM) to explore the atypical neural configuration at every scanning time point in ASD, based on resting-state functional magnetic resonance imaging (rs-fMRI) data from the Autism Brain Imaging Data Exchange. Subsequently, partial least squares regression and pathway enrichment analysis were employed to explore the potential molecular mechanism associated with atypical neural dynamics in ASD. 8 HMM states were inferred from rs-fMRI data. Compared to typically developing, individuals on the autism spectrum showed atypical state-specific temporal characteristics, including number of states and occurrences, mean life time and transition probability between states. Moreover, these atypical temporal characteristics could predict communication difficulties of ASD, and states assoicated with negative activation in default mode network and frontoparietal network, and positive activation in somatomotor network, ventral attention network, and limbic network, had higher predictive contribution. Furthermore, a total of 321 genes was revealed to be significantly associated with atypical dynamic brain states of ASD, and these genes are mainly enriched in neurodevelopmental pathways. Our study provides new insights into characterizing the atypical neural dynamics from a moment-to-moment perspective, and indicates a linkage between atypical neural configuration and gene expression in ASD.

Imbalanced optimal feedback motor control system in spinocerebellar ataxia type 3.

BACKGROUND AND PURPOSE: Human motor planning and control depend highly on optimal feedback control systems, such as the neocortex-cerebellum circuit. Here, diffusion tensor imaging was used to verify the disruption of the neocortex-cerebellum circuit in spinocerebellar ataxia type 3 (SCA3), and the circuit's disruption correlation with SCA3 motor dysfunction was investigated. METHODS: This study included 45 patients with familial SCA3, aged 17-67 years, and 49 age- and sex-matched healthy controls, aged 21-64 years. Tract-based spatial statistics and probabilistic tractography was conducted using magnetic resonance images of the patients and controls. The correlation between the local probability of probabilistic tractography traced from the cerebellum and clinical symptoms measured using specified symptom scales was also calculated. RESULTS: The cerebellum-originated probabilistic tractography analysis showed that structural connectivity, mainly in the subcortical cerebellar-thalamo-cortical tract, was significantly reduced and the cortico-ponto-cerebellar tract was significantly stronger in the SCA3 group than in the control group. The enhanced tract was extended to the right lateral parietal region and the right primary motor cortex. The enhanced neocortex-cerebellum connections were highly associated with disease progression, including duration and symptomatic deterioration. Tractography probabilities from the cerebellar to parietal and sensorimotor areas were significantly negatively correlated with motor abilities in patients with SCA3. CONCLUSION: To our knowledge, this study is the first to reveal that disrupting the neocortex-cerebellum loop can cause SCA3-induced motor dysfunctions. The specific interaction between the cerebellar-thalamo-cortical and cortico-ponto-cerebellar pathways in patients with SCA3 and its relationship with ataxia symptoms provides a new direction for future research.

An Efficient Graph Learning System for Emotion Recognition Inspired by the Cognitive Prior Graph of EEG Brain Network.

Benefiting from the high-temporal resolution of electroencephalogram (EEG), EEG-based emotion recognition has become one of the hotspots of affective computing. For EEG-based emotion recognition systems, it is crucial to utilize state-of-the-art learning strategies to automatically learn emotion-related brain cognitive patterns from emotional EEG signals, and the learned stable cognitive patterns effectively ensure the robustness of the emotion recognition system. In this work, to realize the efficient decoding of emotional EEG, we propose a graph learning system Graph Convolutional Network framework with Brain network initial inspiration and Fused attention mechanism (BF-GCN) inspired by the brain cognitive mechanism to automatically learn graph patterns from emotional EEG and improve the performance of EEG emotion recognition. In the proposed BF-GCN, three graph branches, i.e., cognition-inspired functional graph branch, data-driven graph branch, and fused common graph branch, are first elaborately designed to automatically learn emotional cognitive graph patterns from emotional EEG signals. And then, the attention mechanism is adopted to further capture the brain activation graph patterns that are related to emotion cognition to achieve an efficient representation of emotional EEG signals. Essentially, the proposed BF-CGN model is a cognition-inspired graph learning neural network model, which utilizes the spectral graph filtering theory in the automatic learning and extracting of emotional EEG graph patterns. To evaluate the performance of the BF-GCN graph learning system, we conducted subject-dependent and subject-independent experiments on two public datasets, i.e., SEED and SEED-IV. The proposed BF-GCN graph learning system has achieved 97.44% (SEED) and 89.55% (SEED-IV) in subject-dependent experiments, and the results in subject-independent experiments have achieved 92.72% (SEED) and 82.03% (SEED-IV), respectively. The state-of-the-art performance indicates that the proposed BF-GCN graph learning system has a robust performance in EEG-based emotion recognition, which provides a promising direction for affective computing.

Individualized Structural Perturbations on Normative Brain Connectome Restrict Deep Brain Stimulation Outcomes in Parkinson's Disease.

BACKGROUND: Patients with Parkinson's disease (PD) respond to deep brain stimulation (DBS) variably. However, how brain substrates restrict DBS outcomes remains unclear. OBJECTIVE: In this article, we aim to identify prognostic brain signatures for explaining the response variability. METHODS: We retrospectively investigated a cohort of patients with PD (n = 141) between 2017 and 2022, and defined DBS outcomes as the improvement ratio of clinical motor scores. We used a deviation index to quantify individual perturbations on a reference structural covariance network acquired with preoperative T1-weighted magnetic resonance imaging. The neurobiological perturbations of patients were represented as z scored indices based on the chronological perturbations measured on a group of normal aging adults. RESULTS: After applying stringent statistical tests (z > 2.5) and correcting for false discoveries (P < 0.01), we found that accelerated deviations mainly affected the prefrontal cortex, motor strip, limbic system, and cerebellum in PD. Particularly, a negative network within the accelerated deviations, expressed as "more preoperative deviations, less postoperative improvements," could predict DBS outcomes (mean absolute error = 0.09, R2 = 0.15). Moreover, a fusion of personal brain predictors and medical responses significantly improved traditional evaluations of DBS outcomes. Notably, the most important brain predictor, a pathway connecting the cognitive unit (prefrontal cortex) and motor control unit (cerebellum and motor strip), partially mediates DBS outcomes with the age at surgery. CONCLUSIONS: Our findings suggest that individual structural perturbations on the cognitive motor control circuit are critical for modulating DBS outcomes. Interventions toward the circuit have the potential for additional clinical improvements. © 2024 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Morphometric brain organization across the human lifespan reveals increased dispersion linked to cognitive performance.

The human brain is organized as segregation and integration units and follows complex developmental trajectories throughout life. The cortical manifold provides a new means of studying the brain's organization in a multidimensional connectivity gradient space. However, how the brain's morphometric organization changes across the human lifespan remains unclear. Here, leveraging structural magnetic resonance imaging scans from 1,790 healthy individuals aged 8 to 89 years, we investigated age-related global, within- and between-network dispersions to reveal the segregation and integration of brain networks from 3D manifolds based on morphometric similarity network (MSN), combining multiple features conceptualized as a "fingerprint" of an individual's brain. Developmental trajectories of global dispersion unfolded along patterns of molecular brain organization, such as acetylcholine receptor. Communities were increasingly dispersed with age, reflecting more disassortative morphometric similarity profiles within a community. Increasing within-network dispersion of primary motor and association cortices mediated the influence of age on the cognitive flexibility of executive functions. We also found that the secondary sensory cortices were decreasingly dispersed with the rest of the cortices during aging, possibly indicating a shift of secondary sensory cortices across the human lifespan from an extreme to a more central position in 3D manifolds. Together, our results reveal the age-related segregation and integration of MSN from the perspective of a multidimensional gradient space, providing new insights into lifespan changes in multiple morphometric features of the brain, as well as the influence of such changes on cognitive performance.

Brain development of a school-aged boy with autism spectrum condition talented in arithmetic: a case report.

Whereas autism spectrum condition is known for its social and communicative challenges, some autistic children demonstrate unusual islets of abilities including those related to mathematics, the neurobiological underpinnings of which are increasingly becoming the focus of research. Here we describe an 8-year-old autistic boy with intellectual and language challenges, yet exceptional arithmetic ability. He can perform verbal-based multiplication of three- and even four-digit numbers within 20 seconds. To gain insights into the neural basis of his talent, we investigated the gray matter in the child's brain in comparison to typical development, applying voxel-based morphometry to magnetic resonance imaging data. The case exhibited reduced gray matter volume in regions associated with arithmetic, which may suggest an accelerated development of brain regions with arithmetic compared to typically developing individuals: potentially a key factor contributing to his exceptional talent. Taken together, this case report describes an example of the neurodiversity of autism. Our research provides valuable insights into the potential neural basis of exceptional arithmetic abilities in individuals with the autism spectrum and its potential contribution to depicting the diversity and complexity of autism.

An investigation into the abnormal dynamic connection mechanism of generalized anxiety disorders based on non-homogeneous Markov models.

BACKGROUND: The dynamic and hierarchical nature of the functional brain network. The neural dynamical systems tend to converge to multiple attractors (stable fixed points or dynamical states) in long run. Little is known about how the changes in this brain dynamic "long-term" behavior of the connectivity flow of brain network in generalized anxiety disorder (GAD). METHODS: This study recruited 92 patients with GAD and 77 healthy controls (HC). We applied a reachable probability approach combining a Non-homogeneous Markov model with transition probability to quantify all possible connectivity flows and the hierarchical structure of brain functional systems at the dynamic level and the stationary probability vector (10-step transition probabilities) to describe the steady state of the system in the long run. A random forest algorithm was conducted to predict the severity of anxiety. RESULTS: The dynamic functional patterns in distributed brain networks had larger possibility to converge in bilateral thalamus, posterior cingulate cortex (PCC), right superior occipital gyrus (SOG) and smaller possibility to converge in bilateral superior temporal gyrus (STG) and right parahippocampal gyrus (PHG) in patients with GAD compared to HC. The abnormal transition probability pattern could predict anxiety severity in patients with GAD. LIMITATIONS: Small samples and subjects taking medications may have influenced our results. Future studies are expected to rule out the potential confounding effects. CONCLUSION: Our results have revealed abnormal dynamic neural communication and integration in emotion regulation in patients with GAD, which give new insights to understand the dynamics of brain function of patients with GAD.

Family Environment Modulates Linkage of Transdiagnostic Psychiatric Phenotypes and Dissociable Brain Features in the Developing Brain.

BACKGROUND: Family environment has long been known for shaping brain function and psychiatric phenotypes, especially during childhood and adolescence. Accumulating neuroimaging evidence suggests that across different psychiatric disorders, common phenotypes may share common neural bases, indicating latent brain-behavior relationships beyond diagnostic categories. However, the influence of family environment on the brain-behavior relationship from a transdiagnostic perspective remains unknown. METHODS: We included a community-based sample of 699 participants (ages 5-22 years) and applied partial least squares regression analysis to determine latent brain-behavior relationships from whole-brain functional connectivity and comprehensive phenotypic measures. Comparisons were made between diagnostic and nondiagnostic groups to help interpret the latent brain-behavior relationships. A moderation model was introduced to examine the potential moderating role of family factors in the estimated brain-behavior associations. RESULTS: Four significant latent brain-behavior pairs were identified that reflected the relationship of dissociable brain network and general behavioral problems, cognitive and language skills, externalizing problems, and social dysfunction, respectively. The group comparisons exhibited interpretable variations across different diagnostic groups. A warm family environment was found to moderate the brain-behavior relationship of core symptoms in internalizing disorders. However, in neurodevelopmental disorders, family factors were not found to moderate the brain-behavior relationship of core symptoms, but they were found to affect the brain-behavior relationship in other domains. CONCLUSIONS: Our findings leveraged a transdiagnostic analysis to investigate the moderating effects of family factors on brain-behavior associations, emphasizing the different roles that family factors play during this developmental period across distinct diagnostic groups.

Decomposing cortical activity through neuronal tracing connectome-eigenmodes in marmosets.

Deciphering the complex relationship between neuroanatomical connections and functional activity in primate brains remains a daunting task, especially regarding the influence of monosynaptic connectivity on cortical activity. Here, we investigate the anatomical-functional relationship and decompose the neuronal-tracing connectome of marmoset brains into a series of eigenmodes using graph signal processing. These cellular connectome eigenmodes effectively constrain the cortical activity derived from resting-state functional MRI, and uncover a patterned cellular-functional decoupling. This pattern reveals a spatial gradient from coupled dorsal-posterior to decoupled ventral-anterior cortices, and recapitulates micro-structural profiles and macro-scale hierarchical cortical organization. Notably, these marmoset-derived eigenmodes may facilitate the inference of spontaneous cortical activity and functional connectivity of homologous areas in humans, highlighting the potential generalizing of the connectomic constraints across species. Collectively, our findings illuminate how neuronal-tracing connectome eigenmodes constrain cortical activity and improve our understanding of the brain's anatomical-functional relationship.

Compressed cerebellar functional connectome hierarchy in spinocerebellar ataxia type 3.

Spinocerebellar ataxia type 3 (SCA3) is an inherited movement disorder characterized by a progressive decline in motor coordination. Despite the extensive functional connectivity (FC) alterations reported in previous SCA3 studies in the cerebellum and cerebellar-cerebral pathways, the influence of these FC disturbances on the hierarchical organization of cerebellar functional regions remains unclear. Here, we compared 35 SCA3 patients with 48 age- and sex-matched healthy controls using a combination of voxel-based morphometry and resting-state functional magnetic resonance imaging to investigate whether cerebellar hierarchical organization is altered in SCA3. Utilizing connectome gradients, we identified the gradient axis of cerebellar hierarchical organization, spanning sensorimotor to transmodal (task-unfocused) regions. Compared to healthy controls, SCA3 patients showed a compressed hierarchical organization in the cerebellum at both voxel-level (p < .05, TFCE corrected) and network-level (p < .05, FDR corrected). This pattern was observed in both intra-cerebellar and cerebellar-cerebral gradients. We observed that decreased intra-cerebellar gradient scores in bilateral Crus I/II both negatively correlated with SARA scores (left/right Crus I/II: r = -.48/-.50, p = .04/.04, FDR corrected), while increased cerebellar-cerebral gradients scores in the vermis showed a positive correlation with disease duration (r = .48, p = .04, FDR corrected). Control analyses of cerebellar gray matter atrophy revealed that gradient alterations were associated with cerebellar volume loss. Further FC analysis showed increased functional connectivity in both unimodal and transmodal areas, potentially supporting the disrupted cerebellar functional hierarchy uncovered by the gradients. Our findings provide novel evidence regarding alterations in the cerebellar functional hierarchy in SCA3.

Multi-Semantic Decoding of Visual Perception with Graph Neural Networks.

Constructing computational decoding models to account for the cortical representation of semantic information plays a crucial role in understanding visual perception. The human visual system processes interactive relationships among different objects when perceiving the semantic contents of natural visions. However, the existing semantic decoding models commonly regard categories as completely separate and independent visually and semantically and rarely consider the relationships from prior information. In this work, a novel semantic graph learning model was proposed to decode multiple semantic categories of perceived natural images from brain activity. The proposed model was validated on the functional magnetic resonance imaging data collected from five normal subjects while viewing 2750 natural images comprising 52 semantic categories. The results showed that the Graph Neural Network-based decoding model achieved higher accuracies than other deep neural network models. Moreover, the co-occurrence probability among semantic categories showed a significant correlation with the decoding accuracy. Additionally, the results suggested that semantic content organized in a hierarchical way with higher visual areas was more closely related to the internal visual experience. Together, this study provides a superior computational framework for multi-semantic decoding that supports the visual integration mechanism of semantic processing.

Divergent suicidal symptomatic activations converge on somato-cognitive action network in depression.

Individuals with depression have the highest lifetime prevalence of suicide attempts (SA) among mental illnesses. Numerous neuroimaging studies have developed biomarkers from task-related neural activation in depressive patients with SA, but the findings are inconsistent. Empowered by the contemporary interconnected view of depression as a neural system disorder, we sought to identify a specific brain circuit utilizing published heterogeneous neural activations. We systematically reviewed all published cognitive and emotional task-related functional MRI studies that investigated differences in the location of neural activations between depressive patients with and without SA. We subsequently mapped an underlying brain circuit functionally connecting to each experimental activation using a large normative connectome database (n = 1000). The identified SA-related functional network was compared to the network derived from the disease control group. Finally, we decoded this convergent functional connectivity network using microscale transcriptomic and chemo-architectures, and macroscale psychological processes. We enrolled 11 experimental tasks from eight studies, including depressive patients with SA (n = 147) and without SA (n = 196). The heterogeneous SA-related neural activations localized to the somato-cognitive action network (SCAN), exhibiting robustness to little perturbations and specificity for depression. Furthermore, the SA-related functional network was colocalized with brain-wide gene expression involved in inflammatory and immunity-related biological processes and aligned with the distribution of the GABA and noradrenaline neurotransmitter systems. The findings demonstrate that the SA-related functional network of depression is predominantly located at the SCAN, which is an essential implication for understanding depressive patients with SA.

Macroscale intrinsic dynamics are associated with microcircuit function in focal and generalized epilepsies.

Epilepsies are a group of neurological disorders characterized by abnormal spontaneous brain activity, involving multiscale changes in brain functional organizations. However, it is not clear to what extent the epilepsy-related perturbations of spontaneous brain activity affect macroscale intrinsic dynamics and microcircuit organizations, that supports their pathological relevance. We collect a sample of patients with temporal lobe epilepsy (TLE) and genetic generalized epilepsy with tonic-clonic seizure (GTCS), as well as healthy controls. We extract massive temporal features of fMRI BOLD time-series to characterize macroscale intrinsic dynamics, and simulate microcircuit neuronal dynamics used a large-scale biological model. Here we show whether macroscale intrinsic dynamics and microcircuit dysfunction are differed in epilepsies, and how these changes are linked. Differences in macroscale gradient of time-series features are prominent in the primary network and default mode network in TLE and GTCS. Biophysical simulations indicate reduced recurrent connection within somatomotor microcircuits in both subtypes, and even more reduced in GTCS. We further demonstrate strong spatial correlations between differences in the gradient of macroscale intrinsic dynamics and microcircuit dysfunction in epilepsies. These results emphasize the impact of abnormal neuronal activity on primary network and high-order networks, suggesting a systematic abnormality of brain hierarchical organization.

Transcriptomic Similarity Informs Neuromorphic Deviations in Depression Biotypes.

BACKGROUND: Major depressive disorder (MDD) is complicated by population heterogeneity, motivating the investigation of biotypes through imaging-derived phenotypes. However, neuromorphic heterogeneity in MDD remains unclear, and how the correlated gene expression (CGE) connectome constrains these neuromorphic anomalies in MDD biotypes has not yet been studied. METHODS: Here, we related cortical thickness deviations in MDD biotypes to a pattern of CGE connectome. Cortical thickness was estimated from 3-dimensional T1-weighted magnetic resonance images in 2 independent cohorts (discovery cohort: N = 425; replication cohort: N = 217). The transcriptional activity was measured according to Allen Human Brain Atlas. A density peak-based clustering algorithm was used to identify MDD biotypes. RESULTS: We found that patients with MDD were clustered into 2 replicated biotypes based on single-patient regional deviations from healthy control participants across 2 datasets. Biotype 1 mainly exhibited cortical thinning across the brain, whereas biotype 2 mainly showed cortical thickening in the brain. Using brainwide gene expression data, we found that deviations of transcriptionally connected neighbors predicted regional deviation for both biotypes. Furthermore, putative CGE-informed epicenters of biotype 1 were concentrated on the cognitive control circuit, whereas biotype 2 epicenters were located in the social perception circuit. The patterns of epicenter likelihood were separately associated with depression- and anxiety-response maps, suggesting that epicenters of MDD biotypes may be associated with clinical efficacies. CONCLUSIONS: Our findings linked the CGE connectome and neuromorphic deviations to identify distinct epicenters in MDD biotypes, providing insight into how microscale gene expressions informed MDD biotypes.

Disentangling the Individual-Shared and Individual-Specific Subspace of Altered Brain Functional Connectivity in Autism Spectrum Disorder.

BACKGROUND: Despite considerable effort toward understanding the neural basis of autism spectrum disorder (ASD) using case-control analyses of resting-state functional magnetic resonance imaging data, findings are often not reproducible, largely due to biological and clinical heterogeneity among individuals with ASD. Thus, exploring the individual-shared and individual-specific altered functional connectivity (AFC) in ASD is important to understand this complex, heterogeneous disorder. METHODS: We considered 254 individuals with ASD and 295 typically developing individuals from the Autism Brain Imaging Data Exchange to explore the individual-shared and individual-specific subspaces of AFC. First, we computed AFC matrices of individuals with ASD compared with typically developing individuals. Then, common orthogonal basis extraction was used to project AFC of ASD onto 2 subspaces: an individual-shared subspace, which represents altered connectivity patterns shared across ASD, and an individual-specific subspace, which represents the remaining individual characteristics after eliminating the individual-shared altered connectivity patterns. RESULTS: Analysis yielded 3 common components spanning the individual-shared subspace. Common components were associated with differences of functional connectivity at the group level. AFC in the individual-specific subspace improved the prediction of clinical symptoms. The default mode network-related and cingulo-opercular network-related magnitudes of AFC in the individual-specific subspace were significantly correlated with symptom severity in social communication deficits and restricted, repetitive behaviors in ASD. CONCLUSIONS: Our study decomposed AFC of ASD into individual-shared and individual-specific subspaces, highlighting the importance of capturing and capitalizing on individual-specific brain connectivity features for dissecting heterogeneity. Our analysis framework provides a blueprint for parsing heterogeneity in other prevalent neurodevelopmental conditions.

Gray matter atrophy is constrained by normal structural brain network architecture in depression.

BACKGROUND: There is growing evidence that gray matter atrophy is constrained by normal brain network (or connectome) architecture in neuropsychiatric disorders. However, whether this finding holds true in individuals with depression remains unknown. In this study, we aimed to investigate the association between gray matter atrophy and normal connectome architecture at individual level in depression. METHODS: In this study, 297 patients with depression and 256 healthy controls (HCs) from two independent Chinese dataset were included: a discovery dataset (105 never-treated first-episode patients and matched 130 HCs) and a replication dataset (106 patients and matched 126 HCs). For each patient, individualized regional atrophy was assessed using normative model and brain regions whose structural connectome profiles in HCs most resembled the atrophy patterns were identified as putative epicenters using a backfoward stepwise regression analysis. RESULTS: In general, the structural connectome architecture of the identified disease epicenters significantly explained 44% (±16%) variance of gray matter atrophy. While patients with depression demonstrated tremendous interindividual variations in the number and distribution of disease epicenters, several disease epicenters with higher participation coefficient than randomly selected regions, including the hippocampus, thalamus, and medial frontal gyrus were significantly shared by depression. Other brain regions with strong structural connections to the disease epicenters exhibited greater vulnerability. In addition, the association between connectome and gray matter atrophy uncovered two distinct subgroups with different ages of onset. CONCLUSIONS: These results suggest that gray matter atrophy is constrained by structural brain connectome and elucidate the possible pathological progression in depression.

Cortical thickness reductions associate with brain network architecture in major depressive disorder.

BACKGROUND: Cortical thickness reductions in major depressive disorder are distributed across multiple regions. Research has indicated that cortical atrophy is influenced by connectome architecture on a range of neurological and psychiatric diseases. However, whether connectome architecture contributes to changes in cortical thickness in the same manner as it does in depression is unclear. This study aims to explain the distribution of cortical thickness reductions across the cortex in depression by brain connectome architecture. METHODS: Here, we calculated a differential map of cortical thickness between 110 depression patients and 88 age-, gender-, and education level-matched healthy controls by using T1-weighted images and a structural network reconstructed through the diffusion tensor imaging of control group. We then used a neighborhood deformation model to explore how cortical thickness change in an area is influenced by areas structurally connected to it. RESULTS: We found that cortical thickness in the frontoparietal and default networks decreased in depression, regional cortical thickness changes were related to reductions in their neighbors and were mainly limited by the frontoparietal and default networks, and the epicenter was in the prefrontal lobe. CONCLUSION: Current findings suggest that connectome architecture contributes to the irregular topographic distribution of cortical thickness reductions in depression and cortical atrophy is restricted by and dependent on structural foundation.

Effects of rTMS Intervention on Functional Neuroimaging Activities in Adolescents with Major Depressive Disorder Measured Using Resting-State fMRI.

Repetitive transcranial magnetic stimulation (rTMS) to the left dorsolateral prefrontal cortex (L-DLPFC) is commonly used for the clinical treatment of major depressive disorder (MDD). The neuroimaging biomarkers and mechanisms of rTMS are still not completely understood. This study aimed to explore the functional neuroimaging changes induced by rTMS in adolescents with MDD. A total of ten sessions of rTMS were administrated to the L-DLPFC in thirteen adolescents with MDD once a day for two weeks. All of them were scanned using resting-state functional magnetic resonance imaging at baseline and after rTMS treatment. The regional homogeneity (ReHo), amplitude of low-frequency fluctuation (ALFF), and the subgenual anterior cingulate cortex (sgACC)-based functional connectivity (FC) were computed as neuroimaging indicators. The correlation between changes in the sgACC-based FC and the improvement in depressive symptoms was also analyzed. After rTMS treatment, ReHo and ALFF were significantly increased in the L-DLPFC, the left medial prefrontal cortex, bilateral medial orbital frontal cortex, and the left ACC. ReHo and ALFF decreased mainly in the left middle occipital gyrus, the right middle cingulate cortex (MCC), bilateral calcarine, the left cuneus, and the left superior occipital gyrus. Furthermore, the FCs between the left sgACC and the L-DLPFC, the right IFGoper, the left MCC, the left precuneus, bilateral post-central gyrus, the left supplementary motor area, and the left superior marginal gyrus were enhanced after rTMS treatment. Moreover, the changes in the left sgACC-left MCC FC were associated with an improvement in depressive symptoms in early improvers. This study showed that rTMS treatment in adolescents with MDD causes changes in brain activities and sgACC-based FC, which may provide basic neural biomarkers for rTMS clinical trials.

Advancing nitrate reduction to ammonia: insights into mechanism, activity control, and catalyst design over Pt nanoparticle-based ZrO2.

The reduction of nitrogen oxides (NOx) to NH3, or N2 represents a crucial step in mitigating atmospheric NO3 and NO2 emissions, a significant contributor to air pollution. Among these reduction products, ammonia (NH3) holds particular significance due to its utility in nitrogen-based fertilizers and its versatile applications in various industrial processes. Platinum-based catalysts have exhibited promise in enhancing the rate and selectivity of these reduction reactions. In this study, we employ density functional theory (DFT) calculations to explore the catalytic potential of Pt nanoparticle (PtNP)-supported ZrO2 for the conversion of NO3 to NH3. The most favorable pathway for the NO3 reduction to NH3 follows a sequence, that is, NO3 → NO2 → NO → ONH → ONH2/HNOH → NH2/NH → NH2 → NH3, culminating in the production of valuable ammonia. The introduction of low-state Fe and Co dopants into the ZrO2 support reduces energy barriers for the most challenging rate-determining hydrogenation step in NOx reduction to NH3, demonstrating significant improvements in catalytic activity. The incorporation of dopants into the ZrO2 support results in a depletion of electron density within the Pt cocatalyst resulting in enhanced hydrogen transfer efficiency during the hydrogenation process. This study aims to provide insights into the catalytic activity of platinum-based ZrO2 catalysts and will help design new high-performance catalysts for the reduction of atmospheric pollutants and for energy applications.