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Genetic generalized epilepsy is a network disorder typically involving distributed areas identified by classical neuroanatomy. However, the finer topological relationships in terms of continuous spatial arrangement between these systems are still ambiguous. Connectome gradients provide the topological representations of human macroscale hierarchy in an abstract low-dimensional space by embedding the functional connectome into a set of axes. Leveraging connectome gradients, we systematically scrutinized abnormalities of functional connectome gradient in patients with genetic generalized epilepsy with tonic-clonic seizure (GGE-GTCS, n = 78) compared to healthy controls (HC, n = 85), and further examined the reproducibility across multiple processing configurations and in an independent validation sample (patients with GGE-GTCS, n = 28; HC, n = 31). Our findings demonstrated an extended principal gradient at different spatial scales, network-level and vertex-level, in patients with GGE-GTCS. We found consistent results across processing parameters and in validation sample. The extended principal gradient revealed the excessive functional segregation between unimodal and transmodal systems associated with duration of epilepsy and age at seizure onset in patients. Furthermore, the connectivity profile of regions with abnormal principal gradients verified the disrupted functional hierarchy revealed by gradients. Together, our findings provided a novel view of functional system hierarchy alterations, which facilitated a continuous spatial arrangement of macroscale networks, to increase our understanding of the functional connectome hierarchy in generalized epilepsy.The expectation-suppression effect - reduced stimulus-evoked responses to expected stimuli - is widely considered to be an empirical hallmark of reduced prediction errors in the framework of predictive coding. Here we challenge this notion by proposing that that expectation suppression could be explained by a reduced attention effect. Specifically, we argue that reduced responses to predictable stimuli can also be explained by a reduced saliency-driven allocation of attention. We base our discussion mainly on findings in the visual cortex and propose that resolving this controversy requires the assessment of qualitative differences between the ways in which attention and surprise enhance brain responses.The intrinsic activity of the human brain, observed with resting-state fMRI (rsfMRI) and functional connectivity, exhibits macroscale spatial organization such as functional networks and gradients. Dynamic analysis techniques have shown that functional connectivity is a mere summary of time-varying patterns with distinct spatial and temporal characteristics. A better understanding of these patterns might provide insight into aspects of the brain's intrinsic activity that cannot be inferred by functional connectivity or the spatial maps derived from it, such as functional networks and gradients. Here, we describe three spatiotemporal patterns of coordinated activity across the whole brain obtained by averaging similar ~20-second-long segments of rsfMRI timeseries. In each of these patterns, activity propagates along a particular macroscale functional gradient, simultaneously across the cerebral cortex and in most other brain regions. In some regions, like the thalamus, the propagation suggests previously-undescribed gradients. The coordinated activity across areas is consistent with known tract-based connections, and nuanced differences in the timing of peak activity between regions point to plausible driving mechanisms. The magnitude of correlation within and particularly between functional networks is remarkably diminished when these patterns are regressed from the rsfMRI timeseries, a quantitative demonstration of their significant role in functional connectivity. Taken together, our results suggest that a few recurring patterns of propagating intrinsic activity along macroscale gradients give rise to and coordinate functional connections across the whole brain.Approximately one in five children worldwide suffers from childhood malnutrition and its complications, including increased susceptibility to inflammation and infectious diseases. Due to improved early interventions, most of these children now survive early malnutrition, even in low-resource settings (LRS). However, many continue to exhibit neurodevelopmental deficits, including low IQ, poor school performance, and behavioral problems over their lifetimes. Most studies have relied on neuropsychological tests, school performance, and mental health and behavioral measures. Few studies, in contrast, have assessed brain structure and function, and to date, these have mainly relied on low-cost techniques, including electroencephalography (EEG) and evoked potentials (ERP). The use of more advanced methods of neuroimaging, including magnetic resonance imaging (MRI) and functional near-infrared spectroscopy (fNIRS), has been limited by cost factors and lack of availability of these technologies in developing countries, where malnutrition is nearly ubiquitous. This report summarizes the current state of knowledge and evidence gaps regarding childhood malnutrition and the study of its impact on neurodevelopment. It may help to inform the development of new strategies to improve the identification, classification, and treatment of neurodevelopmental disabilities in underserved populations at the highest risk for childhood malnutrition.Hearing loss is a heterogeneous disorder thought to affect brain reorganization across the lifespan. Here, structural alterations of the brain due to hearing loss are assessed by using unique effect size metrics based on Cohen's d and Hedges' g. These metrics are used to map coordinates of gray matter (GM) and white matter (WM) alterations from bilateral congenital and acquired hearing loss populations. A systematic review and meta-analysis revealed m = 72 studies with structural alterations measured with magnetic resonance imaging (MRI) (bilateral = 64, unilateral = 8). The bilateral studies categorized hearing loss into congenital and acquired cases (n = 7,445) and control cases (n = 2,924), containing 66,545 datapoint metrics. Hearing loss was found to affect GM and underlying WM in nearly every region of the brain. In congenital hearing loss, GM decreased most in the frontal lobe. Similarly, acquired hearing loss had a decrease in frontal lobe GM, albeit the insula was most decreased. In congenital, WM underlying the frontal lobe GM was most decreased. In congenital, the right hemisphere was more negatively impacted than the left hemisphere; however, in acquired, this was the opposite. The WM alterations most frequently underlined GM alterations in congenital hearing loss, while acquired hearing loss studies did not frequently assess the WM metric. Future studies should use the endophenotype of hearing loss as a prognostic template for discerning clinical outcomes.White matter (WM) development early in life is a critical component of brain development that facilitates the coordinated function of neuronal pathways. Additionally, alterations in WM have been implicated in various neurodevelopmental disorders, including psychiatric disorders. Because of the need to understand WM development in the weeks immediately following birth, we characterized changes in WM microstructure throughout the postnatal macaque brain during the first year of life. This is a period in primates during which genetic, developmental, and environmental factors may have long-lasting impacts on WM microstructure. Studies in nonhuman primates (NHPs) are particularly valuable as a model for understanding human brain development because of their evolutionary relatedness to humans. Here, 34 rhesus monkeys (23 females, 11 males) were imaged longitudinally at 3, 7, 13, 25, and 53 weeks of age with T1-weighted (MPnRAGE) and diffusion tensor imaging (DTI). UNC6852 in vitro With linear mixed-effects (LME) modeling, we demonstrated robust logarithmic growth in FA, MD, and RD trajectories extracted from 18 WM tracts across the brain. Estimated rate of change curves for FA, MD, and RD exhibited an initial 10-week period of exceedingly rapid WM development, followed by a precipitous decline in growth rates. K-means clustering of raw DTI trajectories and rank ordering of LME model parameters revealed distinct posterior-to-anterior and medial-to-lateral gradients in WM maturation. Finally, we found that individual differences in WM microstructure assessed at 3 weeks of age were significantly related to those at 1 year of age. This study provides a quantitative characterization of very early WM growth in NHPs and lays the foundation for future work focused on the impact of alterations in early WM developmental trajectories in relation to human psychopathology.Brain age prediction studies aim at reliably estimating the difference between the chronological age of an individual and their predicted age based on neuroimaging data, which has been proposed as an informative measure of disease and cognitive decline. As most previous studies relied exclusively on magnetic resonance imaging (MRI) data, we hereby investigate whether combining structural MRI with functional magnetoencephalography (MEG) information improves age prediction using a large cohort of healthy subjects (N = 613, age 18-88 years) from the Cam-CAN repository. To this end, we examined the performance of dimensionality reduction and multivariate associative techniques, namely Principal Component Analysis (PCA) and Canonical Correlation Analysis (CCA), to tackle the high dimensionality of neuroimaging data. Using MEG features (mean absolute error (MAE) of 9.60 years) yielded worse performance when compared to using MRI features (MAE of 5.33 years), but a stacking model combining both feature sets improved age prediction performance (MAE of 4.88 years). Furthermore, we found that PCA resulted in inferior performance, whereas CCA in conjunction with Gaussian process regression models yielded the best prediction performance. Notably, CCA allowed us to visualize the features that significantly contributed to brain age prediction. We found that MRI features from subcortical structures were more reliable age predictors than cortical features, and that spectral MEG measures were more reliable than connectivity metrics. Our results provide an insight into the underlying processes that are reflective of brain aging, yielding promise for the identification of reliable biomarkers of neurodegenerative diseases that emerge later during the lifespan.

As the population ages, maintaining mental health and well-being of older adults is a public health priority. Beyond objective measures of health, self-perceived quality of life (QoL) is a good indicator of successful aging. In older adults, it has been shown that QoL is related to structural brain changes. However, QoL is a multi-faceted concept and little is known about the specific relationship of each QoL domain to brain structure, nor about the links with other aspects of brain integrity, including white matter microstructure, brain perfusion and amyloid deposition, which are particularly relevant in aging. Therefore, we aimed to better characterize the brain biomarkers associated with each QoL domain using a comprehensive multimodal neuroimaging approach in older adults.

One hundred and thirty-five cognitively unimpaired older adults (mean age±SD 69.4±3.8 y) underwent structural and diffusion magnetic resonance imaging, together with early and late florbetapir positron emission tomography scans. QoL was assessed using the brief version of the World Health Organization's QoL instrument, which allows measuring four distinct domains of QoL self-perceived physical health, psychological health, social relationships and environment.

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