Structural Brain Networks Research Articles

Structural brain connectivity does not associate with childhood trauma in individuals with schizophrenia

BackgroundSchizophrenia is a brain dysconnectivity disorder. However, it is not well understood whether the experience of childhood trauma (CT) affects dysconnectivity in individuals with schizophrenia (SZ). Using a network-based approach, we examined whether self-reported CT would explain additional variance compared to whole-brain topology and structural connectivity changes in SZ versus healthy controls (HC). Material and methodsCT was assessed in 51 SZ (mean age ± standard deviation 44 ± 11 years) and 140 HC (34.0 ± 12 years). Structural brain networks were constructed from T1-weighted MR and diffusion-MRI scans using non-tensor based tractography. Group differences in whole-brain topology and permutation-based statistics were examined and corrected for age and sex. ResultsSZ showed reductions in efficiency, strength, clustering and density (p <0.01) as well as increases in path length (F(range) = 4.71-18.1, p <0.03) when compared to HC. We also observed hypoconnectivity in a subnetwork of frontotemporal, frontoparietal and occipital regions in SZ relative to HC (T > 4.0, p <0.001). However, we did not find that high CT levels were related to structural network differences or structural connectivity changes in SZ. ConclusionsCT did not impact on topology or subnetwork connectivity changes in SZ. High CT levels were also not associated with any differences in network organisation irrespective of diagnosis. However, our findings confirm that SZ showed both network-level reductions and increases in a subnetwork. These findings suggest that the patterns of neuroanatomical dysconnectivity in established schizophrenia may not be influenced by CT. Future studies are needed to investigate the association between CT and structural dysconnectivity in schizophrenia.

Neuro-Immune Communication at the Core of Craving-Associated Brain Structural Network Reconfiguration in Methamphetamine Users

Methamphetamine (MA) use disorder is a chronic neurotoxic brain disease characterized by a high risk of relapse driven by intense cravings. However, the neurobiological signatures of cravings remain unclear, limiting the effectiveness of various treatment methods. Diffusion MRI (dMRI) scans from 62 MA users and 57 healthy controls (HC) were used in this study. The MA users were longitudinally followed up during their period of long-term abstinence (duration of long-term abstinence: 347.52±99.25 days). We systematically quantified the control ability of each brain region for craving-associated state transitions using network control theory from a causal perspective. Craving-associated structural alterations (CSA) were investigated through multivariate group comparisons and biological relevance analysis. The neural mechanisms underlying CSA were elucidated using transcriptomic and neurochemical analyses. We observed that long-term abstinence-induced structural alterations significantly influenced the state transition energy involved in the cognitive control response to external information, which correlated with changes in craving scores (r ∼ 0.35, P <0.01). Our causal network analysis further supported the crucial role of the prefrontal cortex (PFC) in craving mechanisms. Notably, while the PFC is central to the craving, the CSAs were distributed widely across multiple brain regions (PFDR<0.05), with strong alterations in somatomotor regions (PFDR<0.05) and moderate alterations in high-level association networks (PFDR<0.05). Additionally, transcriptomic, chemical compounds, cell-type analyses, and molecular imaging collectively highlight the influence of neuro-immune communication on human craving modulation. Our results offer an integrative, multi-scale perspective on unraveling the neural underpinnings of craving and suggest that neuro-immune signaling may be a promising target for future human addiction therapeutics.

The brain’s structural connectivity and pre-reading abilities in young children with prenatal alcohol exposure

Children with prenatal alcohol exposure (PAE) may develop a range of neurological and behavioral deficits, including reading and language disorders. Studying the brain’s structural connectivity and its relationship to pre-reading/reading skills in young children with PAE can help understand the roots of reading deficits associated with PAE. 363 diffusion MRI scans from 135 children (114 scans from 53 children with PAE) were collected between ages 3–7 years. Children completed NEPSY-II Phonological Processing and Speeded Naming to assess pre-reading skills at each scan. Structural brain network properties were assessed in 16 regions from both hemispheres using graph theory. Linear mixed models were used to account for repeated measures within participants. Children with PAE had significantly lower pre-reading scores than unexposed children, and significantly lower graph theory metrics across bilateral reading networks. Moreover, PAE significantly moderated the associations between Phonological Processing and global efficiency and nodal degree in the bilateral and left hemisphere reading networks, such that children with PAE had stronger associations than unexposed controls. No significant associations were found for Speeded Naming. Our results suggest that brain alterations may underlie early pre-reading difficulties in children with PAE.

Effects of sleep on the glymphatic functioning and multimodal human brain network affecting memory in older adults.

Understanding how sleep affects the glymphatic system and human brain networks is crucial for elucidating the neurophysiological mechanism underpinning aging-related memory declines. We analyzed a multimodal dataset collected through magnetic resonance imaging (MRI) and polysomnographic recording from 72 older adults. A proxy of the glymphatic functioning was obtained from the Diffusion Tensor Image Analysis along the Perivascular Space (DTI-ALPS) index. Structural and functional brain networks were constructed based on MRI data, and coupling between the two networks (SC-FC coupling) was also calculated. Correlation analyses revealed that DTI-ALPS was negatively correlated with sleep quality measures [e.g., Pittsburgh Sleep Quality Index (PSQI) and apnea-hypopnea index]. Regarding human brain networks, DTI-ALPS was associated with the strength of both functional connectivity (FC) and structural connectivity (SC) involving regions such asthe middle temporal gyrus and parahippocampal gyrus, as well as with the SC-FC coupling ofrich-club connections. Furthermore, we found that DTI-ALPS positively mediated the association between sleep quality and rich-club SC-FC coupling. The rich-club SC-FC coupling further mediated the association between DTI-ALPS and memory function in good sleepers but not in poor sleepers. The results suggest a disrupted glymphatic-brain relationship in poor sleepers, which underlies memory decline. Our findings add important evidence that sleep quality affects cognitive health through the underlying neural relationships and the interplay between the glymphatic system and multimodal brain networks.

The cumulative impact of clinical risk on brain networks and associations with executive function impairments in adolescents with congenital heart disease.

Patients with congenital heart disease (CHD) demonstrate altered structural brain network connectivity. However, there is large variability between reported results and little information is available to identify those patients at highest risk for brain alterations. Thus, we aimed to investigate if network connectivity measures were associated with the individual patient's cumulative load of clinical risk factors and with family-environmental factors in a cohort of adolescents with CHD. Further, we investigated associations with executive function impairments. In 53 adolescents with CHD who underwent open-heart surgery during infancy, and 75 healthy controls, diffusion magnetic resonance imaging and neuropsychological assessment was conducted at a mean age of 13.2 ± 1.3 years. Structural connectomes were constructed using constrained spherical deconvolution tractography. Graph theory and network-based statistics were applied to investigate network connectivity measures. A cumulative clinical risk (CCR) score was built by summing up binary risk factors (neonatal, cardiac, neurologic) based on clinically relevant thresholds. The role of family-environmental factors (parental education, parental mental health, and family function) was investigated. An age-adjusted executive function summary score was built from nine neuropsychological tests. While network integration and segregation were preserved in adolescents with CHD, they showed lower edge strength in a dense subnetwork. A higher CCR score was associated with lower network segregation, edge strength, and executive function performance. Edge strength was particularly reduced in a subnetwork including inter-frontal and fronto-parietal-thalamic connections. There was no association with family-environmental factors. Poorer executive functioning was associated with lower network integration and segregation. We demonstrated evidence for alterations of network connectivity strength in adolescents with CHD - particularly in those patients who face a cumulative exposure to multiple clinical risk factors over time. Quantifying the cumulative load of risk early in life may help to better predict trajectories of brain development in order to identify and support the most vulnerable patients as early as possible.

Structural brain network organization in children with prenatal alcohol exposure

IntroductionThere is growing evidence suggesting that children with prenatal alcohol exposure (PAE) struggle with cognitively demanding tasks, such as learning, attention, and language. Complex structural network analyses can provide insight into the neurobiological underpinnings of these functions, as they may be sensitive for characterizing the effects of PAE on the brain. However, investigations on how PAE affects brain networks are limited. We aim to compare diffusion magnetic resonance imaging (MRI) tractography-based structural networks between children with low-to-moderate PAE in trimester 1 only (T1) or throughout all trimesters (T1-T3) with those without alcohol exposure prenatally. MethodsOur cohort included three groups of children aged 6 to 8 years: 1) no PAE (n = 24), 2) low-to-moderate PAE during T1 only (n = 30), 3) low-to-moderate PAE throughout T1-T3 (n = 36). Structural networks were constructed using the multi-shell multi-tissue constrained spherical deconvolution tractography technique. Quantitative group-wise analyses were conducted at three levels: (a) at the whole-brain network level, using both network-based statistical analyses and network centrality; and then using network centrality at (b) the modular level, and (c) per-region level, including the regions identified as brain hubs. ResultsCompared with the no PAE group, widespread brain network alterations were observed in the PAE T1-T3 group using network-based statistics, but no alterations were observed for the PAE T1 group. Network alterations were also detected at the module level in the PAE T1-T3 compared with the no PAE group, with lower eigenvector centrality in the module that closely represented the right cortico-basal ganglia-thalamo-cortical network. No significant group differences were found in network centrality at the per-region level, including the hub regions. ConclusionsThis study demonstrated that low-to-moderate PAE throughout pregnancy may alter brain structural connectivity, which may explain the neurodevelopmental deficits associated with PAE. It is possible that timing and duration of alcohol exposure are crucial, as PAE in T1 only did not appear to alter brain structural connectivity.

MMF-NNs: Multi-modal Multi-granularity Fusion Neural Networks for brain networks and its application to epilepsy identification

Structural and functional brain networks are generated from two scan sequences of magnetic resonance imaging data, which can provide different perspectives for describing pathological changes caused by brain diseases. Recent studies found that fusing these two types of brain networks improves performance in brain disease identification. However, traditional fusion models combine these brain networks at a single granularity, ignoring the natural multi-granularity structure of brain networks that can be divided into the edge, node, and graph levels. To this end, this paper proposes a Multi-modal Multi-granularity Fusion Neural Networks (MMF-NNs) framework for brain networks, which integrates the features of the multi-modal brain network from global (i.e., graph-level) and local (i.e., edge-level and node-level) granularities to take full advantage of the topological information. Specifically, we design an interactive feature learning module at the local granularity to learn feature maps of structural and functional brain networks at the edge-level and the node-level, respectively. In that way, these two types of brain networks are fused during the feature learning process. At the global granularity, a multi-modal decomposition bilinear pooling module is designed to learn the graph-level joint representation of these brain networks. Experiments on real epilepsy datasets demonstrate that MMF-NNs are superior to several state-of-the-art methods in epilepsy identification.

Identifying Brain Network Structure for an fMRI Effective Connectivity Study Using the Least Absolute Shrinkage and Selection Operator (LASSO) Method.

Background: Studying causality relationships between different brain regions using the fMRI method has attracted great attention. To investigate causality relationships between different brain regions, we need to identify both the brain network structure and the influence magnitude. Most current methods concentrate on magnitude estimation, but not on identifying the connection or structure of the network. To address this problem, we proposed a nonlinear system identification method, in which a polynomial kernel was adopted to approximate the relation between the system inputs and outputs. However, this method has an overfitting problem for modelling the input-output relation if we apply the method to model the brain network directly. Methods: To overcome this limitation, this study applied the least absolute shrinkage and selection operator (LASSO) model selection method to identify both brain region networks and the connection strength (system coefficients). From these coefficients, the causality influence is derived from the identified structure. The method was verified based on the human visual cortex with phase-encoded designs. The functional data were pre-processed with motion correction. The visual cortex brain regions were defined based on a retinotopic mapping method. An eight-connection visual system network was adopted to validate the method. The proposed method was able to identify both the connected visual networks and associated coefficients from the LASSO model selection. Results: The result showed that this method can be applied to identify both network structures and associated causalities between different brain regions. Conclusions: System identification with LASSO model selection algorithm is a powerful approach for fMRI effective connectivity study.

Diagnosis of Major Depressive Disorder Based on Individualized Brain Functional and Structural Connectivity.

Traditional neuroimaging studies have primarily emphasized analysis at the group level, often neglecting the specificity at the individual level. Recently, there has been a growing interest in individual differences in brain connectivity. Investigating individual-specific connectivity is important for understanding the mechanisms of major depressive disorder (MDD) and the variations among individuals. To integrate individualized functional connectivity and structural connectivity with machine learning techniques to distinguish people with MDD and healthy controls (HCs). Prospective. A total of 182 patients with MDD and 157 HCs and a verification cohort including 54 patients and 46 HCs. 3.0 T/T1-weighted imaging, resting-state functional MRI with echo-planar sequence, and diffusion tensor imaging with single-shot spin echo. Functional and structural brain networks from rs-fMRI and DTI data were constructed, respectively. Based on these networks, individualized functional connectivity (IFC) and individualized structural connectivity (ISC) were extracted using common orthogonal basis extraction (COBE). Subsequently, multimodal canonical correlation analysis combined with joint independent component analysis (mCCA + jICA) was conducted to fusion analysis to identify the joint and unique independent components (ICs) across multiple modes. These ICs were utilized to generate features, and a support vector machine (SVM) model was implemented for the classification of MDD. The differences in individualized connectivity between patients and controls were compared using two-sample t test, with a significance threshold set at P < 0.05. The established model was tested and evaluated using the receiver operating characteristic (ROC) curve. The classification performance of the constructed individualized connectivity feature model after multisequence fusion increased from 72.2% to 90.3%. Furthermore, the prediction model showed significant predictive power for assessing the severity of depression in patients with MDD (r = 0.544). The integration of IFC and ISC through multisequence fusion enhances our capacity to identify MDD, highlighting the advantages of the individualized approach and underscoring its significance in MDD research. 1 TECHNICAL EFFICACY: Stage 2.

Distributed associations among white matter hyperintensities and structural brain networks with fluid cognition in healthy aging

White matter hyperintensities (WMHs) are associated with age-related cognitive impairment and increased risk of Alzheimer’s disease. However, the manner by which WMHs contribute to cognitive impairment is unclear. Using a combination of predictive modeling and network neuroscience, we investigated the relationship between structural white matter connectivity and age, fluid cognition, and WMHs in 68 healthy adults (18–78 years). Consistent with previous work, WMHs were increased in older adults and exhibited a strong negative association with fluid cognition. Extending previous work, using predictive modeling, we demonstrated that age, WMHs, and fluid cognition were jointly associated with widespread alterations in structural connectivity. Subcortical-cortical connections between the thalamus/basal ganglia and frontal and parietal regions of the default mode and frontoparietal networks were most prominent. At the network level, both age and WMHs were negatively associated with network density and communicability, and positively associated with modularity. Spatially, WMHs were most prominent in arterial zones served by the middle cerebral artery and associated lenticulostriate branches that supply subcortical regions. Finally, WMHs overlapped with all major white matter tracts, most prominently in tracts that facilitate subcortical-cortical communication and are implicated in fluid cognition, including the anterior thalamic-radiations and forceps minor. Finally, results of mediation analyses suggest that whole-brain WMH load influences age-related decline in fluid cognition. Thus, across multiple levels of analysis, we showed that WMHs were increased in older adults and associated with altered structural white matter connectivity and network topology involving subcortical-cortical pathways critical for fluid cognition.

Involvement of the cerebellum in structural connectivity enhancement in episodic migraine

BackgroundThe pathophysiology of migraine remains poorly understood, yet a growing number of studies have shown structural connectivity disruptions across large-scale brain networks. Although both structural and functional changes have been found in the cerebellum of migraine patients, the cerebellum has barely been assessed in previous structural connectivity studies of migraine. Our objective is to investigate the structural connectivity of the entire brain, including the cerebellum, in individuals diagnosed with episodic migraine without aura during the interictal phase, compared with healthy controls.MethodsTo that end, 14 migraine patients and 15 healthy controls were recruited (all female), and diffusion-weighted and T1-weighted MRI data were acquired. The structural connectome was estimated for each participant based on two different whole-brain parcellations, including cortical and subcortical regions as well as the cerebellum. The structural connectivity patterns, as well as global and local graph theory metrics, were compared between patients and controls, for each of the two parcellations, using network-based statistics and a generalized linear model (GLM), respectively. We also compared the number of connectome streamlines within specific white matter tracts using a GLM.ResultsWe found increased structural connectivity in migraine patients relative to healthy controls with a distinct involvement of cerebellar regions, using both parcellations. Specifically, the node degree of the posterior lobe of the cerebellum was greater in patients than in controls and patients presented a higher number of streamlines within the anterior limb of the internal capsule. Moreover, the connectomes of patients exhibited greater global efficiency and shorter characteristic path length, which correlated with the age onset of migraine.ConclusionsA distinctive pattern of heightened structural connectivity and enhanced global efficiency in migraine patients compared to controls was identified, which distinctively involves the cerebellum. These findings provide evidence for increased integration within structural brain networks in migraine and underscore the significance of the cerebellum in migraine pathophysiology.

Study of a precise treatment protocol for patients with consciousness disorders based on the brain network analysis of functional magnetic resonance imaging.

How to conduct objective and accurate individualized assessments of patients with disorders of consciousness (DOC) and carry out precision rehabilitation treatment technology is a major rehabilitation problem that needs to be solved urgently. In this study, a multi-layer brain network was constructed based on functional magnetic resonance imaging (fMRI) to analyze the structural and functional brain networks of patients with DOC at different levels and to find regulatory targets (imaging markers) with recovery potential for DOC. Then repeated transcranial magnetic stimulation (rTMS) was performed in DOC patients to clinically validate. The brain network connectivity of DOC patients with different consciousness states is different, and the most obvious brain regions appeared in the olfactory cortex and precuneus. rTMS stimulation could effectively improve the consciousness level of DOC patients and stimulate the occipital lobe (specific regions found in this study) and the dorsolateral prefrontal cortex (DLPFC), and both parts had a good consciousness recovery effect. In clinical work, personalized stimulation regimen treatment combined with the brain network characteristics of DOC patients can improve the treatment effect.

Schizophrenia and Neurodevelopment: Insights From Connectome Perspective.

Schizophrenia is conceptualized as a brain connectome disorder that can emerge as early as late childhood and adolescence. However, the underlying neurodevelopmental basis remains unclear. Recent interest has grown in children and adolescent patients who experience symptom onset during critical brain development periods. Inspired by advanced methodological theories and large patient cohorts, Chinese researchers have made significant original contributions to understanding altered brain connectome development in early-onset schizophrenia (EOS). We conducted a search of PubMed and Web of Science for studies on brain connectomes in schizophrenia and neurodevelopment. In this selective review, we first address the latest theories of brain structural and functional development. Subsequently, we synthesize Chinese findings regarding mechanisms of brain structural and functional abnormalities in EOS. Finally, we highlight several pivotal challenges and issues in this field. Typical neurodevelopment follows a trajectory characterized by gray matter volume pruning, enhanced structural and functional connectivity, improved structural connectome efficiency, and differentiated modules in the functional connectome during late childhood and adolescence. Conversely, EOS deviates with excessive gray matter volume decline, cortical thinning, reduced information processing efficiency in the structural brain network, and dysregulated maturation of the functional brain network. Additionally, common functional connectome disruptions of default mode regions were found in early- and adult-onset patients. Chinese research on brain connectomes of EOS provides crucial evidence for understanding pathological mechanisms. Further studies, utilizing standardized analyses based on large-sample multicenter datasets, have the potential to offer objective markers for early intervention and disease treatment.

Pathologic Substrates of Structural Brain Network Resilience and Topology in Parkinson Disease Decedents.

In Parkinson disease (PD), α-synuclein spreading through connected brain regions leads to neuronal loss and brain network disruptions. With diffusion-weighted imaging (DWI), it is possible to capture conventional measures of brain network organization and more advanced measures of brain network resilience. We aimed to investigate which neuropathologic processes contribute to regional network topologic changes and brain network resilience in PD. Using a combined postmortem MRI and histopathology approach, PD and control brain donors with available postmortem in situ 3D T1-weighted MRI, DWI, and brain tissue were selected from the Netherlands Brain Bank and Normal Aging Brain Collection Amsterdam. Probabilistic tractography was performed, and conventional network topologic measures of regional eigenvector centrality and clustering coefficient, and brain network resilience (change in global efficiency upon regional node failure) were calculated. PSer129 α-synuclein, phosphorylated-tau, β-amyloid, neurofilament light-chain immunoreactivity, and synaptophysin density were quantified in 8 cortical regions. Group differences and correlations were assessed with rank-based nonparametric tests, with age, sex, and postmortem delay as covariates. Nineteen clinically defined and pathology-confirmed PD (7 F/12 M, 81 ± 7 years) and 15 control (8 F/7 M, 73 ± 9 years) donors were included. With regional conventional measures, we found lower eigenvector centrality only in the parahippocampal gyrus in PD (d = -1.08, 95% CI 0.003-0.010, p = 0.021), which did not associate with underlying pathology. No differences were found in regional clustering coefficient. With the more advanced measure of brain network resilience, we found that the PD brain network was less resilient to node failure of the dorsal anterior insula compared with the control brain network (d = -1.00, 95% CI 0.0012-0.0015, p = 0.018). This change was not directly driven by neuropathologic processes within the dorsal anterior insula or in connected regions but was associated with higher Braak α-synuclein staging (rs = -0.40, p = 0.036). Although our cohort might suffer from selection bias, our results highlight that regional network disturbances are more complex to interpret than previously believed. Regional neuropathologic processes did not drive regional topologic changes, but a global increase in α-synuclein pathology had a widespread effect on brain network reorganization in PD.

Modality-Aware Discriminative Fusion Network for Integrated Analysis of Brain Imaging Genomics.

Mild cognitive impairment (MCI) represents an early stage of Alzheimer's disease (AD), characterized by subtle clinical symptoms that pose challenges for accurate diagnosis. The quest for the identification of MCI individuals has highlighted the importance of comprehending the underlying mechanisms of disease causation. Integrated analysis of brain imaging and genomics offers a promising avenue for predicting MCI risk before clinical symptom onset. However, most existing methods face challenges in: 1) mining the brain network-specific topological structure and addressing the single nucleotide polymorphisms (SNPs)-related noise contamination and 2) extracting the discriminative properties of brain imaging genomics, resulting in limited accuracy for MCI diagnosis. To this end, a modality-aware discriminative fusion network (MA-DFN) is proposed to integrate the complementary information from brain imaging genomics to diagnose MCI. Specifically, we first design two modality-specific feature extraction modules: the graph convolutional network with edge-augmented self-attention module (GCN-EASA) and the deep adversarial denoising autoencoder module (DAD-AE), to capture the topological structure of brain networks and the intrinsic distribution of SNPs. Subsequently, a discriminative-enhanced fusion network with correlation regularization module (DFN-CorrReg) is employed to enhance inter-modal consistency and between-class discrimination in brain imaging and genomics. Compared to other state-of-the-art approaches, MA-DFN not only exhibits superior performance in stratifying cognitive normal (CN) and MCI individuals but also identifies disease-related brain regions and risk SNPs locus, which hold potential as putative biomarkers for MCI diagnosis.

MULTIMODAL NEURAL CORRELATES OF CHILDHOOD PSYCHOPATHOLOGY.

Complex structural and functional changes occurring in typical and atypical development necessitate multidimensional approaches to better understand the risk of developing psychopathology. Here, we simultaneously examined structural and functional brain network patterns in relation to dimensions of psychopathology in the Adolescent Brain Cognitive Development dataset. Several components were identified, recapitulating the psychopathology hierarchy, with the general psychopathology (p) factor explaining most covariance with multimodal imaging features, while the internalizing, externalizing, and neurodevelopmental dimensions were each associated with distinct morphological and functional connectivity signatures. Connectivity signatures associated with the p factor and neurodevelopmental dimensions followed the sensory-to-transmodal axis of cortical organization, which is related to the emergence of complex cognition and risk for psychopathology. Results were consistent in two separate data subsamples, supporting generalizability, and robust to variations in analytical parameters. Our findings help in better understanding biological mechanisms underpinning dimensions of psychopathology, and could provide brain-based vulnerability markers.

Human adolescent brain similarity development is different for paralimbic versus neocortical zones

Adolescent development of human brain structural and functional networks is increasingly recognized as fundamental to emergence of typical and atypical adult cognitive and emotional proodal magnetic resonance imaging (MRI) data collected from N [Formula: see text] 300 healthy adolescents (51%; female; 14 to 26 y) each scanned repeatedly in an accelerated longitudinal design, to provide an analyzable dataset of 469 structural scans and 448 functional MRI scans. We estimated the morphometric similarity between each possible pair of 358 cortical areas on a feature vector comprising six macro- and microstructural MRI metrics, resulting in a morphometric similarity network (MSN) for each scan. Over the course of adolescence, we found that morphometric similarity increased in paralimbic cortical areas, e.g., insula and cingulate cortex, but generally decreased in neocortical areas, and these results were replicated in an independent developmental MRI cohort (N [Formula: see text] 304). Increasing hubness of paralimbic nodes in MSNs was associated with increased strength of coupling between their morphometric similarity and functional connectivity. Decreasing hubness of neocortical nodes in MSNs was associated with reduced strength of structure-function coupling and increasingly diverse functional connections in the corresponding fMRI networks. Neocortical areas became more structurally differentiated and more functionally integrative in a metabolically expensive process linked to cortical thinning and myelination, whereas paralimbic areas specialized for affective and interoceptive functions became less differentiated, as hypothetically predicted by a developmental transition from periallocortical to proisocortical organization of the cortex. Cytoarchitectonically distinct zones of the human cortex undergo distinct neurodevelopmental programs during typical adolescence.

Regional brain structural network topology mediates the associations between white matter damage and disease severity in first-episode, Treatment-naïve pubertal children with major depressive disorder

Puberty is a vulnerable period for the onset of major depressive disorder (MDD) due to considerable neurodevelopmental changes. Prior diffusion tensor imaging (DTI) studies in depressed youth have had heterogeneous participants, making assessment of early pathology challenging due to illness chronicity and medication confounds. This study leveraged whole-brain DTI and graph theory approaches to probe white matter (WM) abnormalities and disturbances in structural network topology related to first-episode, treatment-naïve pediatric MDD. Participants included 36 first-episode, unmedicated adolescents with MDD (mean age 15.8 years) and 29 age- and sex-matched healthy controls (mean age 15.2 years). Compared to controls, the MDD group showed reduced fractional anisotropy in the internal and external capsules, unveiling novel regions of WM disruption in early-onset depression. The right thalamus and superior temporal gyrus were identified as network hubs where betweenness centrality changes mediated links between WM anomalies and depression severity. A diagnostic model incorporating demographics, DTI, and network metrics achieved an AUROC of 0.88 and a F1 score of 0.80 using a neural network algorithm. By examining first-episode, treatment-naïve patients, this work identified novel WM abnormalities and a potential causal pathway linking WM damage to symptom severity via regional structural network alterations in brain hubs.

Contributions of network structure, chemoarchitecture and diagnostic categories to transitions between cognitive topographies.

The mechanisms linking the brain's network structure to cognitively relevant activation patterns remain largely unknown. Here, by leveraging principles of network control, we show how the architecture of the human connectome shapes transitions between 123 experimentally defined cognitive activation maps (cognitive topographies) from the NeuroSynth meta-analytic database. Specifically, we systematically integrated large-scale multimodal neuroimaging data from functional magnetic resonance imaging, diffusion tractography, cortical morphometry and positron emission tomography to simulate how anatomically guided transitions between cognitive states can be reshaped by neurotransmitter engagement or by changes in cortical thickness. Our model incorporates neurotransmitter-receptor density maps (18 receptors and transporters) and maps of cortical thickness pertaining to a wide range of mental health, neurodegenerative, psychiatric and neurodevelopmental diagnostic categories (17,000 patients and 22,000 controls). The results provide a comprehensive look-up table charting how brain network organization and chemoarchitecture interact to manifest different cognitive topographies, and establish a principled foundation for the systematic identification of ways to promote selective transitions between cognitive topographies.

Peripheral and central pathogenesis of postherpetic neuralgia.

Postherpetic neuralgia (PHN) is a classic chronic condition with multiple signs of peripheral and central neuropathy. Unfortunately, the pathogenesis of PHN is not well defined, limiting clinical treatment and disease management. To describe the peripheral and central pathological axes of PHN, including peripheral nerve injury, inflammation induction, central nervous system sensitization, and brain functional and structural network activity. A bibliographic survey was carried out, selecting relevant articles that evaluated the characterization of the pathogenesis of PHN, including peripheral and central pathological axes. Currently, due to the complexity of the pathophysiological mechanisms of PHN and the incomplete understanding of the exact mechanism of neuralgia. It is essential to conduct in-depth research to clarify the origins of PHN pathogenesis and explore effective and comprehensive therapies for PHN.