Cerebral cortex最新文献

Fine sensory modalities play an essential role in perceiving the world. However, little is known about how the cortico-cortical distinguishes between dynamic and static tactile signals. This study investigated oscillatory connectivity during a tactile discrimination task of dynamic and static stimulation via electroencephalogram (EEG) recordings and the fast oscillatory networks across widespread cortical regions. While undergoing EEG recordings, the subject felt an electro-tactile presented by a 3-dot array. Each block consisted of 3 forms of stimulation: Spatio-temporal (dynamic), Spatial (static), and Control condition (lack of electrical stimulation). The average event-related potential for the Spatial and Spatio-temporal conditions exhibited statistically significant differences between 25 and 75, 81 and 121, 174 and 204 and 459 and 489 ms after stimulus onset. Based on those times, the sLORETA approach was used to reconstruct the inverse solutions of EEG. Source localization appeared superior parietal at around 25 to 75 ms, in the primary motor cortex at 81 to 121 ms, in the central prefrontal cortex at 174 to 204 and 459 to 489 ms. To better assess spectral brain functional connectivity, we selected frequency ranges with correspondingly significant differences: for static tactile stimulation, these are concentrated in the Theta, Alpha, and Gamma bands, whereas for dynamic stimulation, the relative energy change bands are focused on the Theta and Alpha bands. These nodes' functional connectivity analysis (phase lag index) showed 3 distinct distributed networks. A tactile information discrimination network linked the Occipital lobe, Prefrontal lobe, and Postcentral gyrus. A tactile feedback network linked the Prefrontal lobe, Postcentral gyrus, and Temporal lobe. A dominant motor feedforward loop network linked the Parietal cortex, Prefrontal lobe, Frontal lobe, and Parietal cortex. Processing dynamic and static tactile signals involves discriminating tactile information, motion planning, and cognitive decision processing.

Effective cognitive performance often requires the allocation of additional neural resources (i.e. blood-oxygen-level-dependent [BOLD] activation) as task demands increase, and this demand-related modulation is affected by amyloid-beta deposition and normal aging. The present study investigated these complex relationships between amyloid, modulation, and cognitive function (i.e. fluid ability). Participants from the Dallas Lifespan Brain Study (DLBS, n = 252, ages 50-89) completed a semantic judgment task during functional magnetic resonance imaging (fMRI) where the judgments differed in classification difficulty. Amyloid burden was assessed via positron emission tomography (PET) using 18F-florbetapir. A quadratic relationship between amyloid standardized value uptake ratios (SUVRs) and BOLD modulation was observed such that modulation was weaker in those with moderately elevated SUVRs (e.g. just reaching amyloid-positivity), whereas those with very high SUVRs (e.g. SUVR > 1.5) showed strong modulation. Greater modulation was related to better fluid ability, and this relationship was strongest in younger participants and those with lower amyloid burden. These results support the theory that effective demand-related modulation contributes to healthy cognitive aging, especially in the transition from middle age to older adulthood, whereas high modulation may be dysfunctional in those with substantial amyloid deposition.

Arithmetic, a high-order cognitive ability, show marked individual difference over development. Despite recent advancements in neuroimaging techniques have enabled the identification of brain markers for individual differences in high-order cognitive abilities, it remains largely unknown about the brain markers for arithmetic. This study used a data-driven connectome-based prediction model to identify brain markers of arithmetic skills from arithmetic-state functional connectivity and individualized structural similarity in 132 children aged 8 to 15 years. We found that both subtraction-state functional connectivity and individualized SS successfully predicted subtraction and multiplication skills but multiplication-state functional connectivity failed to predict either skill. Among the four successful prediction models, most predictive connections were located in frontal-parietal, default-mode, and secondary visual networks. Further computational lesion analyses revealed the essential structural role of frontal-parietal network in predicting subtraction and the essential functional roles of secondary visual, language, and ventral multimodal networks in predicting multiplication. Finally, a few shared nodes but largely nonoverlapping functional and structural connections were found to predict subtraction and multiplication skills. Altogether, our findings provide new insights into the brain markers of arithmetic skills in children and highlight the importance of studying different connectivity modalities and different arithmetic domains to advance our understanding of children's arithmetic skills.

Glaucoma and Alzheimer's disease are critical degenerative neuropathies with global impact. Previous studies have indicated that glaucomatous damage could extend beyond ocular structures, leading to brain alterations potentially associated with Alzheimer's disease risk. This study aimed to explore the causal associations among glaucoma, brain alterations, and Alzheimer's disease. We conducted a comprehensive investigation into the genetic correlation and causality between glaucoma, glaucoma endophenotypes, cerebral cortical surficial area and thickness, and Alzheimer's disease (including late-onset Alzheimer's disease, cognitive performance, and reaction time) using linkage disequilibrium score regression and Mendelian randomization. This study showed suggestive genetic correlations between glaucoma, cortical structures, and Alzheimer's disease. The genetically predicted all-caused glaucoma was nominally associated with a decreased risk of Alzheimer's disease (OR = 0.96, 95% CI: 0.93-0.99, P = 0.013). We found evidence for suggestive causality between glaucoma (endophenotypes) and 20 cortical regions and between 29 cortical regions and Alzheimer's disease (endophenotypes). Four cortical regions were causally associated with cognitive performance or reaction time at a significant threshold (P < 6.2E-04). Thirteen shared cortical regions between glaucoma (endophenotypes) and Alzheimer's disease (endophenotypes) were identified. Our findings complex causal relationships among glaucoma, cerebral cortical structures, and Alzheimer's disease. More studies are required to clarify the mediation effect of cortical alterations in the relationship between glaucoma and Alzheimer's disease.

Working memory is the fundamental function of the various cognitive processes and abilities in the overall trajectory of development. Significant advances in multivariate analysis of human functional magnetic resonance imaging data have converged functional segregation models toward integrated representation-based models. However, due to the inherent limitations of the multi-voxel pattern analysis method, we are unable to determine whether the underlying neural representations are spatially similar in the brain. Our study attempts to answer this question by examining the spatial similarity of brain activity during the working memory task in children and adults. Our results reveal similar patterns of activity between the regions involved in working memory. This functional network of similar spatial patterns was observed in both normally developing children and adults. However, the between-region similarity was more pronounced in adults than in children and associated with better performance. We propose an exchange of similar information flows through the brain at an integrated level of working memory processes, underpinning the holistic nature of working memory representation.

The occurrence mechanism of intracerebral hemorrhage remains unclear. Several recent studies have highlighted the close relationship between environmental senses and intracerebral hemorrhage, but the mechanisms of causal mediation are inconclusive. We aimed to investigate the causal relationships and potential mechanisms between environmental senses and intracerebral hemorrhage. Multiple Mendelian randomization methods were used to identify a causal relationship between environmental senses and intracerebral hemorrhage. Gut microbiota and brain imaging phenotypes were used to find possible mediators. Enrichment and molecular interaction analyses were used to identify potential mediators and molecular targets. No causal relationship between temperature and visual perception with intracerebral hemorrhage was found, whereas long-term noise was identified as a risk factor for intracerebral hemorrhage (OR 2.95, 95% CI: 1.25 to 6.93, PIVW = 0.01). The gut microbiota belonging to the class Negativicutes and the order Selenomonadales and the brain image-derived phenotypes ICA100 node 54, edge 803, edge 1149, and edge 1323 played mediating roles. "Regulation of signaling and function in synaptic organization" is the primary biological pathway of noise-induced intracerebral hemorrhage, and ARHGAP22 may be the critical gene. This study emphasized the importance of environmental noise in the prevention, disease management, and underlying biological mechanisms of intracerebral hemorrhage.

Audiovisual (AV) interaction has been shown in many studies of auditory cortex. However, the underlying processes and circuits are unclear because few studies have used methods that delineate the timing and laminar distribution of net excitatory and inhibitory processes within areas, much less across cortical levels. This study examined laminar profiles of neuronal activity in auditory core (AC) and parabelt (PB) cortices recorded from macaques during active discrimination of conspecific faces and vocalizations. We found modulation of multi-unit activity (MUA) in response to isolated visual stimulation, characterized by a brief deep MUA spike, putatively in white matter, followed by mid-layer MUA suppression in core auditory cortex; the later suppressive event had clear current source density concomitants, while the earlier MUA spike did not. We observed a similar facilitation-suppression sequence in the PB, with later onset latency. In combined AV stimulation, there was moderate reduction of responses to sound during the visual-evoked MUA suppression interval in both AC and PB. These data suggest a common sequence of afferent spikes, followed by synaptic inhibition; however, differences in timing and laminar location may reflect distinct visual projections to AC and PB.

Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta plaques initiated approximately 2 decades before the symptom onset followed by build-up and spreading of neurofibrillary tau aggregates. Although it has been suggested that the amyloid-beta amplifies tau spreading the observed spatial disparity called it into question. Yet, it is unclear how neocortical amyloid-beta remotely affects early pathological tau, triggering it to leave the early formation area, and how amyloid-beta facilitates tau aggregate spreading throughout cortical regions. I aimed to investigate how amyloid-beta can facilitate tau spreading through neuronal connections in the Alzheimer's disease pathological process by combining functional magnetic resonance imaging normative connectomes and longitudinal in vivo molecular imaging data. In total, the imaging data of 317 participants, including 173 amyloid-beta-negative non-demented and 144 amyloid-beta -positive non-demented participants, have entered the study from Alzheimer's Disease Neuroimaging Initiative. Furthermore, normative resting-state functional magnetic resonance imaging connectomes were used to model tau spreading through functional connections. It was observed that the amyloid-beta in regions with the highest deposition (amyloid-beta epicenter) is remotely associated with connectivity-based spreading of tau pathology. Moreover, amyloid-beta in regions that exhibit the highest tau pathology (tau epicenter) is associated with increased connectivity-based tau spreading to non-epicenter regions. The findings provide a further explanation for a long-standing question of how amyloid-beta can affect tau aggregate spreading through neuronal connections despite spatial incongruity. The results suggest that amyloid-beta pathology can remotely and locally facilitate connectivity-based spreading of tau aggregates.