Cerebral asymmetry is a core principle of human brain organization, showing dynamic changes across the lifespan and alterations in brain disorders. However, it remains unclear whether lifespan trajectories of asymmetry differ across populations. We compared lifespan structural asymmetry normative charts of 221 cerebral imaging phenotypes from 43,037 Chinese and 56,339 Western participants aged 0–100 years. The two populations showed distinct lifespan asymmetry patterns in 26.2% of the phenotypes. Chinese-minus-Western asymmetry difference curves displayed distinct patterns across brain phenotypes: rightward (45.7%), leftward (26.2%), rightward-to-leftward (11.8%), leftward-to-rightward (10.0%), and unclassified (6.3%). Population-matched normative models outperformed population-unmatched normative models in capturing normal asymmetry variability among healthy individuals and in detecting abnormal asymmetry deviations in patients with Alzheimer’s disease, mild cognitive impairment, schizophrenia, and major depressive disorder. These findings indicate that population mismatch can bias chart-based individual-level asymmetry assessment and underscore the need for population-representative brain asymmetry normative charts.

Objective Our aim was to conduct a comprehensive meta-analysis of structural neuroimaging studies investigating white matter (WM) microarchitecture and gray matter volume (GMV) abnormalities in patients with autism spectrum disorder (ASD). Methods Totally 24 diffusion tensor imaging studies using tract-based spatial statistics (TBSS) or voxel-based analysis (VBA) approach were included in this meta-analysis. The discrepancies in WM fractional anisotropy, mean diffusivity, axial diffusivity and radial diffusivity between ASD patients and typically developing (TD) individuals and the results of two common methods were compared. Besides, we detect GMV alternations by analyzing 44 voxel-based morphometry studies in ASD and comparing the difference in different developing stages. Results Compared with TD, ASD exhibited significantly WM microstructure alterations in corpus callosum, cortico-spinal projections, anterior thalamic projections, superior longitudinal fasciculus and middle cerebellar peduncles. There is some heterogeneity in aberrant WM microstructure between the TBSS and VBA subgroup. ASD had increased GMV in gyrus rectus, superior and inferior temporal gyrus, and precentral gyrus, and decreased GMV in cerebellum, anterior cingulate/paracingulate gyri, cingulum, and inferior parietal gyri. ASD displayed an age-related trajectory of brain morphometry. Conclusion Our main findings reveal the variable WM microarchitecture and GMV in ASD and offer a neuroanatomical framework that may guide multimodal and longitudinal research.

Abnormalities in resting-state brain activity have been demonstrated in depression patients with different ages, yet the age-related changes in dynamics of brain activity in depression are still limited. Here, we investigated the impacts of age on dynamics of brain activity and the molecular architecture. Resting-state functional magnetic resonance images were obtained from 138 first-episode depression patients and 120 healthy volunteers. All the participants were classified into two age cohorts, including adolescents and adults. Two-way analysis of variance was performed to examine the effect of age on dynamic amplitude of low-frequency fluctuations (ALFF) in depression. Then, cross-modal correlation analyses between dynamic ALFF and neurotransmitter maps were established. Significant diagnosis-by-age interaction of dynamic ALFF was located in medial frontal gyrus, supplementary motor area, postcentral gyrus, paracentral lobule and rolandic operculum. Dynamic ALFF alterations in the diagnosis-by-age interaction effect were associated with serotonergic, dopaminergic, noradrenergic, and GABAergic systems. These findings highlight the interaction between depression and age in brain functional and molecular neuroimaging signatures, which may be useful for future treatment strategies of different ages of depression.

Human brain charts provide unprecedented opportunities for decoding neurodevelopmental milestones and establishing clinical benchmarks for precision brain medicine 1-7. However, current lifespan brain charts are primarily derived from European and North American cohorts, with Asian populations severely underrepresented. Here, we present the first population-specific brain charts for China, developed through the Chinese Lifespan Brain Mapping Consortium (Phase I) using neuroimaging data from 43,037 participants (aged 0-100 years) across 384 sites nationwide. We establish the lifespan normative trajectories for 296 structural brain phenotypes, encompassing global, subcortical, and cortical measures. Cross-population comparisons with Western brain charts (based on data from 56,339 participants aged 0-100 years) reveal distinct neurodevelopmental patterns in the Chinese population, including prolonged cortical and subcortical maturation, accelerated cerebellar growth, and earlier development of sensorimotor regions relative to paralimbic regions. Crucially, these Chinese-specific charts outperform Western-derived models in predicting healthy brain phenotypes and detecting pathological deviations in Chinese clinical cohorts. These findings highlight the urgent need for diverse, population-representative brain charts to advance equitable precision neuroscience and improve clinical validity across populations.

This study investigates abnormalities in cerebellar-cerebral static and dynamic functional connectivity among patients with acute pontine infarction, examining the relationship between these connectivity changes and behavioral dysfunction. Resting-state functional magnetic resonance imaging was utilized to collect data from 45 patients within seven days post-pontine infarction and 34 normal controls. Seed-based static and dynamic functional connectivity analyses identified divergences in cerebellar-cerebral connectivity features between pontine infarction patients and normal controls. Correlations between abnormal functional connectivity features and behavioral scores were explored. Compared to normal controls, left pontine infarction patients exhibited significantly increased static functional connectivity within the executive, affective-limbic, and motor networks. Conversely, right pontine infarction patients demonstrated decreased static functional connectivity in the executive, affective-limbic, and default mode networks, alongside an increase in the executive and motor networks. Decreased temporal variability of dynamic functional connectivity was observed in the executive and default mode networks among left pontine infarction patients. Furthermore, abnormalities in static and dynamic functional connectivity within the executive network correlated with motor and working memory performance in patients. These findings suggest that alterations in cerebellar-cerebral static and dynamic functional connectivity could underpin the behavioral dysfunctions observed in acute pontine infarction patients.

Potential changes in patterns of dynamic functional network connections at the cerebellar-cerebral level in pontine infarction (PI) patients remain unclear. The study aimed to investigate the abnormal patterns of dynamic functional connectivity (dFC) between the cerebellar subregions within networks and regions of the cerebral cortex in patients with PI. Forty-six chronic left pontine infarction (LPI), 32 chronic right pontine infarction (RPI), and 50 healthy controls (HCs) were recruited to undergo resting-state fMRI scans. Cerebellar-cerebral dFC was characterized using the sliding window method and seed-based connectivity analyses. Correlations between altered dFC values and clinical variables (The Rey Auditory Verbal Learning Test and Flanker task) in PI patients and healthy controls were investigated. Compared with HCs, the PI groups showed significantly aberrant cerebellar-cerebral dFC between cerebellar subregions within networks and supratentorial cerebral cortex, including executive, default-mode, and motor networks. Furthermore, Correlation analysis showed a decoupling between abnormal dFC and cognitive functions in PI patients. These findings indicate that PI patients are accompanied by damage to cerebellar subregions within networks and cerebellar-cerebral pathways, which may provide a potential target for treatment or an indication of therapeutic efficacy.

Background Internal capsule strokes often result in multidomain cognitive impairments across memory, attention, and executive function, typically due to disruptions in brain network connectivity. Our study examines these impairments by analyzing interactions within the triple-network model, focusing on both static and dynamic aspects. Methods We collected resting-state fMRI data from 62 left (CI_L) and 56 right (CI_R) internal capsule stroke patients, along with 57 healthy controls (HC). Using independent component analysis to extract the default mode (DMN), executive control (ECN), and salience networks (SAN), we conducted static and dynamic functional network connectivity analyses (DFNC) to identify differences between stroke patients and controls. For DFNC, we used k-means clustering to focus on temporal properties and multilayer network analysis to examine integration and modularity Q, where integration represents dynamic interactions between networks, and modularity Q measures how well the network is divided into distinct modules. We then calculated the correlations between SFNC/DFNC properties with significant inter-group differences and cognitive scales. Results Compared to HC, both CI_L and CI_R patients showed increased static FCs between SAN and DMN and decreased dynamic interactions between ECN and other networks. CI_R patients also had heightened static FCs between SAN and ECN and maintained a state with strongly positive FNCs across all networks in the triple-network model. Additionally, CI_R patients displayed decreased modularity Q. Conclusion These findings highlight that stroke can result in the disruption of static and dynamic interactions in the triple network model, aiding our understanding of the neuropathological basis for multidomain cognitive deficits after internal capsule stroke.

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Background Numerous studies have underscored the presence of abnormal intrinsic neural activity (INA) in individuals with depression. However, recognizing that the age stage may influence the pathophysiology of depression, our study sought to delve into the interplay of depression and age on INA and molecular architecture. Methods One hundred and thirty-eight first-episode depression patients and 120 healthy controls (HC) were recruited and underwent resting-state functional magnetic resonance imaging. The participants were stratified into four groups based on age. Utilizing amplitude of low-frequency fluctuation (ALFF) analyses, we employed an ANCOVA to compare INA patterns in four groups. Additionally, we conducted correlation analyses between ALFF and neurotransmitter maps to elucidate molecular underpinnings of INA abnormalities. Results In comparison to adolescents with early-onset depression and adult HC, adult-onset depression exhibited increased ALFF in the right paracentral lobule. Conversely, early-onset depression, when contrasted with adolescent HC, displayed reduced ALFF in the right paracentral lobule. The interactive brain regions affected by ALFF alterations were associated with serotonergic, GABAergic, and opioid neurotransmitter systems. Limitations The present study was limited to its cross-sectional design. Conclusions This study illuminates an antagonistic effect of depression and age on brain activity in paracentral lobule and provides molecular underpinnings of the corresponding INA abnormalities related to key neurotransmitter systems. These insights may prove valuable in the development of neuromarkers for clinical intervention and treatment of depression.

Background: Subcortical stroke may significantly alter the cerebral cortical structure and affect attention function, but the details of this process remain unclear. The study aimed to investigate the neural substrates underlying attention impairment in patients with subcortical stroke. Materials and Methods: In this prospective observational study, two distinct datasets were acquired to identify imaging biomarkers underlying attention deficit. The first dataset consisted of 86 patients with subcortical stroke, providing a cross-sectional perspective, whereas the second comprised 108 patients with stroke, offering longitudinal insights. All statistical analyses were subjected to false discovery rate correction upon P < 0.05. Results: In the chronic-stage data, the stroke group exhibited significantly poorer attention function compared with that of the control group. The cortical structure analysis showed that patients with stroke exhibited decreased cortical thickness of the precentral gyrus and surface area of the cuneus, along with an increase in various frontal, occipital, and parietal cortices regions. The declined attention function positively correlated with the superior frontal gyrus cortical thickness and supramarginal gyrus surface area. In the longitudinal dataset, patients with stroke showed gradually increasing cortical thickness and surface area within regions of obvious structural reorganization. Furthermore, deficient attention positively correlated with supramarginal gyrus surface area both at the subacute and chronic stages post-stroke. Conclusions: Subcortical stroke can elicit dynamic reorganization of cortical areas associated with attention impairment. Moreover, the altered surface area of the supramarginal gyrus is a potential neuroimaging biomarker for attention deficits.

ObjectiveThe purpose of the study was to investigate the abnormality both of static spontaneous brain activity and dynamic temporal variances following a pontine infarction. MethodsForty-six patients with chronic left pontine infarction (LPI), thirty-two patients with chronic right pontine infarction (RPI), and fifty healthy controls (HCs) were recruited for the study. The static amplitude of low-frequency fluctuations (sALFF), static regional homogeneity (sReHo), dynamic ALFF (dALFF), and dynamic ReHo (dReHo) were employed to detect the alterations in brain activity induced by an infarction. The Rey Auditory Verbal Learning Test and Flanker task were used to evaluate the verbal memory and visual attention function, respectively. Receiver operating characteristic curve analysis was used to reveal the potential capacity of these metrics to distinguish the patients from HCs. ResultsThere were significant variations of these static and dynamic metrics in patients with chronic pontine infarction. The altered regions involved the supratentorial regions, including cortex and subcortical. Moreover, the altered metrics were significantly correlated with verbal memory and visual attention. In addition, these static and dynamic metrics also showed potential in distinguishing stroke patients with behavior deficits from HCs. ConclusionThe pontine infarction-induced cerebral activation changes are observed in both motor and cognitive systems, indicating the functional damage and reorganization across the global cerebral level in these patients with subtentorial infarction, and there is a reciprocal effect between motor and cognitive impairment and repair.

The risk for motor and cognitive impairment is increased in patients with chronic pontine infarction (PI). In this study, we attempted to explore the alterations of neurovascular coupling (NVC) in order to understand the neural basis of behavioral impairment after PI. Three-dimensional pseudo-continuous arterial spin labeling (3D-pcASL) and resting-state functional magnetic resonance imaging (rs-fMRI) were applied in 49 patients with unilateral PI (left-sided, n = 26; right-sided, n = 23) and 30 matched normal subjects to assess whole-brain cerebral blood flow (CBF) and functional connectivity strength (FCS). We evaluated NVC in each subject by calculating the correlation coefficient between the whole-brain CBF and FCS (CBF-FCS coupling) and the ratio between voxel-wise CBF and FCS (CBF/FCS ratio). The FCS maps were then divided into long-range and short-range FCS to identify the influence of connection distance. The results indicated that the CBF-FCS coupling in the whole-brain level was significantly interrupted in PI patients, and the CBF/FCS ratio in cognition-related brain regions was abnormal. Distance-dependent results demonstrated that PI had a more serious effect on long-range neuro-vascular coupling. Correlation analysis revealed that the changes in neurovascular coupling were correlated with working memory scores. These findings imply that disruption of neurovascular coupling in the remote-infarction brain regions may underlie the impaired cognitive functions in chronic PI.

IntroductionThe objective of this study was to characterize the alteration patterns of dynamic spatiotemporal activity in chronic subcortical stroke patients with varying motor outcomes, while investigating the imaging indicators relevant to the assessment of potential cognitive deficits in these patients.MethodsA total of 136 patients and 88 normal controls were included in the analysis of static and dynamic intrinsic brain activity, determined by amplitude of low-frequency fluctuations.ResultsThe findings unveiled that subcortical stroke patients exhibited significantly aberrant temporal dynamics of intrinsic brain activity, involving regions within multiple brain networks. These spatiotemporal patterns were found to be contingent upon the side of the lesion. In addition, these aberrant metrics demonstrated potential in discerning cognitive deficits in stroke patients with memory impairment, with the dynamic indices exerting more influence than the static ones. The observe findings may indicate that subcortical stroke can trigger imbalances in the segregation and integration of spatiotemporal patterns across the entire brain with multi-domain networks, especially in patients with poor motor outcomes.ConclusionIt suggests that the temporal dynamics indices of intrinsic brain activity could serve as potential imaging indicators for assessing cognitive impairment in patients with chronic subcortical stroke, which may be associated with the motor outcomes.

To investigate potential alterations of white matter hyperintensities (WMHs) on J-edited MR spectroscopy (MRS) measures of the primary inhibitory neurotransmitter γ-aminobutyric acid (GABA). Twenty-four WMHs patients and 20 healthy controls (HCs) were recruited to undergo magnetic resonance spectroscopy (MRS) scan at 3T from voxels in left centrum semiovale white matter, using the MEGA point resolved spectroscopy (MEGA-PRESS) technique with the MATLAB-based Gannet tool to estimate GABA+ co-edited macromolecule (GABA+) levels and using Tarquin software to estimate levels of glutamate + glutamine (Glx), total N-acetylaspartate (tNAA), total choline (tCho), and total creatine (tCr). Independent t-tests or Mann-Whitney U-tests were used to test group differences between WMHs and HCs. Additionally, WMHs patients were divided into mild and moderate-severe WMHs subgroup according to the Fazekas scale. Analysis of variance (ANOVA) and post-hoc tests were used among WMHs subgroups and HCs. We found there was a significant reduction in GABA+ levels (p = 0.018) in WMHs patients compared with healthy controls. In subgroup analyses, there was also a significant reduction of GABA+ levels in moderate-severe WMHs subgroup (p = 0.037) and mild WMHs subgroup (p = 0.047) when compared to HCs. Besides, the moderate-severe WMHs subgroup had significantly higher levels of tCho compared with healthy controls (p = 0.019). In conclusion, reduced GABA+ levels in WMHs patients and elevated tCho levels in moderate-severe WMHs were observed when compared with HCs. These results demonstrate that abnormalities of the GABAergic system and choline metabolism may contribute to the pathogenesis of WMHs.

To explore the mechanisms of cognitive impairment and reorganization in patients with left- and right-sided capsular stroke (CS_L, CS_R), we collected resting-state fMRI data from 62 CS_L, 56 CS_R patients and 57 normal controls (NC). Based on the triple-network model [involving the default mode, central executive and salience networks], static (SFNC) and dynamic functional network connectivities (DFNC) were performed to calculate inter-network functional connectivities and estimate temporal features in each state among the three groups. We found more significant SFNC and DFNC changes in CS_R group, suggesting more extensive cognitive impairment and reorganization in CS_R patients than those with CS_L.

Cognitive dysfunction in patients with infratentorial stroke has been paid little attention. Brainstem stroke may disrupt network connectivity across the whole brain and affect multidomain cognition, but the details of this process remain unclear. The study aimed to investigate the effects of stroke-induced pontine injury on whole-brain network connectivity and cognitive function. We included 47 patients with pontine stroke and 56 healthy comparisons (HC), who underwent cognitive tests and functional magnetic resonance imaging (fMRI). Seven meaningful brain networks were identified using independent component analysis (ICA). Patients with pontine stroke had decreased intra-network functional connectivities (FCs) in the primary perceptual and higher cognitive control networks, including sensorimotor network (SMN), visual network (VIS), default mode network (DMN), and salience network (SAN), as well as decreased inter-network FCs in the primary perceptual (VIS-SMN) and higher cognitive control networks (bilateral frontoparietal networks, rFPN-lFPN). While the FCs between the primary perceptual and higher cognitive control networks (VIS-DMN, VIS-rFPN, VIS-lFPN) were increased. Furthermore, the alterations in these FCs correlated with patients' cognitive measurements. These findings suggested that the infratentorial stroke can induce dysfunctional connectivity in both primary perceptual and higher cognitive control networks at the whole-brain level, which may be attributable to the neural substrates of multidomain cognitive deficits in these patients.

Objectives To investigate the longitudinal changes in gray matter volume (GMV) and functional connectivity (FC) in patients with pontine infarction (PI) during a 6-month follow-up period. Methods Twenty-two patients underwent MRI scans and behavioral assessments at 1 week, 1 month, 3 months, and 6 months after PI. Twenty-two normal controls (NC) were administered once with a similar examination. Voxel-wise GMV analysis was used to investigate the difference between the 1 week of PI and NC groups. Longitudinal changes in GMV were assessed and then used as seed regions to explore the accompanying FC changes during the 6-month follow-up. Correlations of the behavioral scores with the imaging indices of clusters with altered GMV and FC were also investigated. Results The LPI group exhibited GMV atrophy in the left cerebellar Crus II, right cerebellar lobule VI, right Vermis VI, while the RPI group showed GMV atrophy in the left cerebellar Crus II. The significant decrease of GMV firstly appeared at 1 month and gradually decreased over time. When using brain regions with GMV atrophy as seeds, longitudinal analysis of FC showed a significant decrease between the left cerebellar Crus II and left middle frontal gyrus at 6 months in the LPI group. Furthermore, the longitudinally altered FC values were negatively correlated with motor scores over time. Conclusion These findings provide evidence for progressive GMV atrophy in the cerebellum and impaired relative FC in patients with PI, which could provide vital information for investigating neural bases of behavioral recovery in PI.

Several functional magnetic resonance imaging (fMRI) studies have demonstrated abnormalities in static intra- and interhemispheric functional connectivity among diverse brain regions in patients with major depressive disorder (MDD). However, the dynamic changes in intra- and interhemispheric functional connectivity patterns in patients with MDD remain unclear. Fifty-eight first-episode, drug-naive patients with MDD and 48 age-, sex-, and education level-matched healthy controls (HCs) underwent resting-state fMRI. Whole-brain functional connectivity, analyzed using the functional connectivity density (FCD) approach, was decomposed into ipsilateral and contralateral functional connectivity. We computed the intra- and interhemispheric dynamic FCD (dFCD) using a sliding window analysis to capture the dynamic patterns of functional connectivity. The temporal variability in functional connectivity was quantified as the variance of the dFCD over time. In addition, intra- and interhemispheric static FCD (sFCD) patterns were calculated. Associations between the dFCD variance and sFCD in abnormal brain regions and the severity of depressive symptoms were analyzed. Compared to HCs, patients with MDD showed lower interhemispheric dFCD variability in the inferior/middle frontal gyrus and decreased sFCD in the medial prefrontal cortex/anterior cingulate cortex and posterior cingulate cortex/precuneus in both intra- and interhemispheric comparisons. No significant correlations were found between any abnormal dFCD variance or sFCD at the intra- and interhemispheric levels and the severity of depressive symptoms. Our results suggest intra- and interhemispheric functional connectivity alterations in the dorsolateral prefrontal cortex (DLPFC) and default mode network regions involved in cognition, execution and emotion. Furthermore, our study emphasizes the essential role of altered interhemispheric communication dynamics in the DLPFC in patients with MDD. These findings contribute to our understanding of the pathophysiology of MDD.

Neurological deficits after stroke are closely related to white matter microstructure damage. However, secondary changes in white matter microstructure after pontine infarction (PI) in the whole brain remain unclear. This study aimed to investigate the correlation of diffusion kurtosis imaging (DKI)-derived diffusion and kurtosis parameters of abnormal white matter tracts with behavioral function in patients with chronic PI. Overall, 60 patients with unilateral chronic PI (33 patients with left PI and 27 patients with right PI) and 30 normal subjects were recruited and underwent DKI scans. Diffusion parameters derived from diffusion tensor imaging (DTI) and DKI and kurtosis parameters derived from DKI were obtained. Between-group differences in multiple parameters were analyzed to assess the changes in abnormal white matter microstructure. Moreover, we also calculated the sensitivities of different diffusion and kurtosis parameters of DTI and DKI for identifying abnormal white matter tracts. Correlations between the DKI-derived parameters in secondary microstructure changes and behavioral scores in the PI were analyzed. Compared with the NC group, both left PI and right PI groups showed more extensive perilesional and remote white matter microstructure changes. The DKI-derived diffusion parameters showed higher sensitivities than did the DTI-derived parameters. Further, DKI-derived diffusion and kurtosis parameters in abnormal white matter regions were correlated with impaired motor and cognitive function in patients with PI. In conclusion, PI could lead to extensive white matter tracts impairment in perilesional and remote regions. Further, the diffusion and kurtosis parameters could be complementary for identifying comprehensive tissue microstructural damage after PI.

Recent neuroimaging studies have shown the possibility of cognitive impairment after pontine stroke. In this study, we aimed to use voxel-mirrored homotopic connectivity (VMHC) to investigate changes in the cognitive function in chronic pontine stroke. Functional MRI (fMRI) and behavioral assessments of cognitive function were obtained from 56 patients with chronic pontine ischemic stroke [28 patients with left-sided pontine stroke (LP) and 28 patients with right-sided pontine stroke (RP)] and 35 matched healthy controls (HC). The one-way ANOVA test was performed for the three groups after the VMHC analysis. Results showed that there were significant decreases in the bilateral lingual gyrus (Lingual_L and Lingual_R) and the left precuneus (Precuneus_L) in patients with chronic pontine ischemic stroke compared to HCs. However, in a post-hoc multiple comparison test, this difference remained only between the HC and RP groups. Moreover, we explored the relationship between the decreased z -values in VMHC and the behavior-task scores using a Pearson's correlation test and found that both scores of short-term memory and long-term memory in the Rey Auditory Verbal Learning Test were positively correlated with z -values of the left lingual gyrus (Lingual_L), the right lingual gyrus (Lingual_R), and the left precuneus (Precuneus_L) in VMHC. Besides that, the z -values of Precuneus_L in VMHC were also negatively correlated with the reaction time for correct responses in the Flanker task and the spatial memory task. In conclusion, first, the lingual gyrus played an important role in verbal memory. Second, the precuneus influenced the working memory, both auditory-verbal memory and visual memory. Third, the right-sided stroke played a greater role in the results of this study. This study provides a basis for further elucidation of the characteristics and mechanisms of cognitive impairment after pontine stroke.