Network Neuroscience最新文献

Capturing and tracking large-scale brain activity dynamics holds the potential to deepen our understanding of cognition. Previously, tools from topological data analysis, especially Mapper, have been successfully used to mine brain activity dynamics at the highest spatiotemporal resolutions. Even though it is a relatively established tool within the field of topological data analysis, Mapper results are highly impacted by parameter selection. Given that noninvasive human neuroimaging data (e.g., from fMRI) is typically fraught with artifacts and no gold standards exist regarding "true" state transitions, we argue for a thorough examination of Mapper parameter choices to better reveal their impact. Using synthetic data (with known transition structure) and real fMRI data, we explore a variety of parameter choices for each Mapper step, thereby providing guidance and heuristics for the field. We also release our parameter exploration toolbox as a software package to make it easier for scientists to investigate and apply Mapper to any dataset.

Time-varying changes in whole-brain connectivity patterns, or connectome state dynamics, are a prominent feature of brain activity with broad functional implications. While infraslow (<0.1 Hz) connectome dynamics have been extensively studied with fMRI, rapid dynamics highly relevant for cognition are poorly understood. Here, we asked whether rapid electrophysiological connectome dynamics constitute subject-specific brain traits and to what extent they are under genetic influence. Using source-localized EEG connectomes during resting state (N = 928, 473 females), we quantified the heritability of multivariate (multistate) features describing temporal or spatial characteristics of connectome dynamics. States switched rapidly every ∼60-500 ms. Temporal features were heritable, particularly Fractional Occupancy (in theta, alpha, beta, and gamma bands) and Transition Probability (in theta, alpha, and gamma bands), representing the duration spent in each state and the frequency of state switches, respectively. Genetic effects explained a substantial proportion of the phenotypic variance of these features: Fractional Occupancy in beta (44.3%) and gamma (39.8%) bands and Transition Probability in theta (38.4%), alpha (63.3%), beta (22.6%), and gamma (40%) bands. However, we found no evidence for the heritability of dynamic spatial features, specifically states' Modularity and connectivity pattern. We conclude that genetic effects shape individuals' connectome dynamics at rapid timescales, specifically states' overall occurrence and sequencing.

Striatum, the input stage of the basal ganglia, is important for sensory-motor integration, initiation and selection of behavior, as well as reward learning. Striatum receives glutamatergic inputs from mainly cortex and thalamus. In rodents, the striatal projection neurons (SPNs), giving rise to the direct and the indirect pathway (dSPNs and iSPNs, respectively), account for 95% of the neurons, and the remaining 5% are GABAergic and cholinergic interneurons. Interneuron axon terminals as well as local dSPN and iSPN axon collaterals form an intricate striatal network. Following chronic dopamine depletion as in Parkinson's disease (PD), both morphological and electrophysiological striatal neuronal features have been shown to be altered in rodent models. Our goal with this in silico study is twofold: (a) to predict and quantify how the intrastriatal network connectivity structure becomes altered as a consequence of the morphological changes reported at the single-neuron level and (b) to investigate how the effective glutamatergic drive to the SPNs would need to be altered to account for the activity level seen in SPNs during PD. In summary, we predict that the richness of the connectivity motifs in the striatal network is significantly decreased during PD while, at the same time, a substantial enhancement of the effective glutamatergic drive to striatum is present.

Different whole-brain computational models have been recently developed to investigate hypotheses related to brain mechanisms. Among these, the Dynamic Mean Field (DMF) model is particularly attractive, combining a biophysically realistic model that is scaled up via a mean-field approach and multimodal imaging data. However, an important barrier to the widespread usage of the DMF model is that current implementations are computationally expensive, supporting only simulations on brain parcellations that consider less than 100 brain regions. Here, we introduce an efficient and accessible implementation of the DMF model: the FastDMF. By leveraging analytical and numerical advances-including a novel estimation of the feedback inhibition control parameter and a Bayesian optimization algorithm-the FastDMF circumvents various computational bottlenecks of previous implementations, improving interpretability, performance, and memory use. Furthermore, these advances allow the FastDMF to increase the number of simulated regions by one order of magnitude, as confirmed by the good fit to fMRI data parcellated at 90 and 1,000 regions. These advances open the way to the widespread use of biophysically grounded whole-brain models for investigating the interplay between anatomy, function, and brain dynamics and to identify mechanistic explanations of recent results obtained from fine-grained neuroimaging recordings.

The neurodegenerative progression of Parkinson's disease affects brain structure and function and, concomitantly, alters the topological properties of brain networks. The network alteration accompanied by motor impairment and the duration of the disease has not yet been clearly demonstrated in the disease progression. In this study, we aim to resolve this problem with a modeling approach using the reduced Jansen-Rit model applied to large-scale brain networks derived from cross-sectional MRI data. Optimizing whole-brain simulation models allows us to discover brain networks showing unexplored relationships with clinical variables. We observe that the simulated brain networks exhibit significant differences between healthy controls (n = 51) and patients with Parkinson's disease (n = 60) and strongly correlate with disease severity and disease duration of the patients. Moreover, the modeling results outperform the empirical brain networks in these clinical measures. Consequently, this study demonstrates that utilizing the simulated brain networks provides an enhanced view of network alterations in the progression of motor impairment and identifies potential biomarkers for clinical indices.

Several recent studies have optimized deep neural networks to learn high-dimensional relationships linking structural and functional connectivity across the human connectome. However, the extent to which these models recapitulate individual-specific characteristics of resting-state functional brain networks remains unclear. A core concern relates to whether current individual predictions outperform simple benchmarks such as group averages and null conditions. Here, we consider two measures to statistically evaluate whether functional connectivity predictions capture individual effects. We revisit our previously published functional connectivity predictions for 1,000 healthy adults and provide multiple lines of evidence supporting that our predictions successfully capture subtle individual-specific variation in connectivity. While predicted individual effects are statistically significant and outperform several benchmarks, we find that effect sizes are small (i.e., 8%-11% improvement relative to group-average benchmarks). As such, initial expectations about individual prediction performance expressed by us and others may require moderation. We conclude that individual predictions can significantly outperform appropriate benchmark conditions and we provide several recommendations for future studies in this area. Future studies should statistically assess the individual prediction performance of their models using one of the measures and benchmarks provided here.

Low-intensity transcranial ultrasound stimulation (TUS) is a noninvasive technique that safely alters neural activity, reaching deep brain areas with good spatial accuracy. We investigated the effects of TUS in macaques using a recent metric, the synergy minus redundancy rank gradient, which quantifies different kinds of neural information processing. We analyzed this high-order quantity on the fMRI data after TUS in two targets: the supplementary motor area (SMA-TUS) and the frontal polar cortex (FPC-TUS). The TUS produced specific changes at the limbic network at FPC-TUS and the motor network at SMA-TUS and altered the sensorimotor, temporal, and frontal networks in both targets, mostly consistent across macaques. Moreover, there was a reduction in the structural and functional coupling after both stimulations. Finally, the TUS changed the intrinsic high-order network topology, decreasing the modular organization of the redundancy at SMA-TUS and increasing the synergistic integration at FPC-TUS.

Time-varying changes in whole-brain connectivity patterns, or connectome state dynamics, hold significant implications for cognition. However, connectome dynamics at fast (>1 Hz) timescales highly relevant to cognition are poorly understood due to the dominance of inherently slow fMRI in connectome studies. Here, we investigated the behavioral significance of rapid electrophysiological connectome dynamics using source-localized EEG connectomes during resting state (N = 926, 473 females). We focused on dynamic connectome features pertinent to individual differences, specifically those with established heritability: Fractional Occupancy (i.e., the overall duration spent in each recurrent connectome state) in beta and gamma bands and Transition Probability (i.e., the frequency of state switches) in theta, alpha, beta, and gamma bands. Canonical correlation analysis found a significant relationship between the heritable phenotypes of subsecond connectome dynamics and cognition. Specifically, principal components of Transition Probabilities in alpha (followed by theta and gamma bands) and a cognitive factor representing visuospatial processing (followed by verbal and auditory working memory) most notably contributed to the relationship. We conclude that rapid connectome state transitions shape individuals' cognitive abilities and traits. Such subsecond connectome dynamics may inform about behavioral function and dysfunction and serve as endophenotypes for cognitive abilities.

Despite the widespread exploration and availability of parcellations for the functional connectome, parcellations designed for the structural connectome are comparatively limited. Current research suggests that there may be no single "correct" parcellation and that the human brain is intrinsically a multiresolution entity. In this work, we propose the Continuous Structural Connectivitity-based, Nested (CoCoNest) family of parcellations-a fully data-driven, multiresolution family of parcellations derived from structural connectome data. The CoCoNest family is created using agglomerative (bottom-up) clustering and error-complexity pruning, which strikes a balance between the complexity of each parcellation and how well it preserves patterns in vertex-level, high-resolution connectivity data. We draw on a comprehensive battery of internal and external evaluation metrics to show that the CoCoNest family is competitive with or outperforms widely used parcellations in the literature. Additionally, we show how the CoCoNest family can serve as an exploratory tool for researchers to investigate the multiresolution organization of the structural connectome.

We generated asynchronous functional networks (aFNs) using a novel method called optimal causation entropy and compared aFN topology with the correlation-based synchronous functional networks (sFNs), which are commonly used in network neuroscience studies. Functional magnetic resonance imaging (fMRI) time series from 212 participants of the National Consortium on Alcohol and Neurodevelopment in Adolescence study were used to generate aFNs and sFNs. As a demonstration of how aFNs and sFNs can be used in tandem, we used multivariate mixed effects models to determine whether age interacted with node efficiency to influence connection probabilities in the two networks. After adjusting for differences in network density, aFNs had higher global efficiency but lower local efficiency than the sFNs. In the aFNs, nodes with the highest outgoing global efficiency tended to be in the brainstem and orbitofrontal cortex. aFN nodes with the highest incoming global efficiency tended to be members of the default mode network in sFNs. Age interacted with node global efficiency in aFNs and node local efficiency in sFNs to influence connection probability. We conclude that the sFN and aFN both offer information about functional brain connectivity that the other type of network does not.