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The critical brain hypothesis states that biological neuronal networks, because of their structural and functional architecture, work near phase transitions for optimal response to internal and external inputs. Criticality thus provides optimal function and behavioral capabilities. We test this hypothesis by examining the influence of brain injury (strokes) on the criticality of neural dynamics estimated at the level of single participants using directly measured individual structural connectomes and whole-brain models. Lesions engender a sub-critical state that recovers over time in parallel with behavior. The improvement of criticality is associated with the re-modeling of specific white-matter connections. We show that personalized whole-brain dynamical models poised at criticality track neural dynamics, alteration post-stroke, and behavior at the level of single participants. The authors investigate the influence of brain injury (strokes) on the criticality of neural dynamics using directly measured connectomes and whole-brain models. They show that lesions engender a sub-critical state that recovers over time in parallel with behavior. [ABSTRACT FROM AUTHOR]

The critical brain hypothesis has emerged as an attractive framework to understand neuronal activity, but it is still widely debated. In this work, we analyze data from a multi-electrodes array in the rat's cortex and we find that power-law neuronal avalanches satisfying the crackling-noise relation coexist with spatial correlations that display typical features of critical systems. In order to shed a light on the underlying mechanisms at the origin of these signatures of criticality, we introduce a paradigmatic framework with a common stochastic modulation and pairwise linear interactions inferred from our data. We show that in such models power-law avalanches that satisfy the crackling-noise relation emerge as a consequence of the extrinsic modulation, whereas scale-free correlations are solely determined by internal interactions. Moreover, this disentangling is fully captured by the mutual information in the system. Finally, we show that analogous power-law avalanches are found in more realistic models of neural activity as well, suggesting that extrinsic modulation might be a broad mechanism for their generation. [ABSTRACT FROM AUTHOR]

Human cognitive abilities are limited resources. Today, in the age of cheap information—cheap to produce, to manipulate, to disseminate—this cognitive bottleneck translates into hypercompetition for rewarding outcomes among actors. These incentives push actors to mutualistically interact with specific memes, seeking the virality of their messages. In turn, memes' chances to persist and spread are subject to changes in the communication environment. In spite of all this complexity, here we show that the underlying architecture of empirical actor-meme information ecosystems evolves into recurring emergent patterns. We then propose an ecology-inspired modelling framework, bringing to light the precise mechanisms causing the observed flexible structural reorganisation. The model predicts—and the data confirm—that users' struggle for visibility induces a re-equilibration of the network's mesoscale towards self-similar nested arrangements. Our final microscale insights suggest that flexibility at the structural level is not mirrored at the dynamical one. Human perceptual and cognitive abilities are limited resources and consequently cheaply available information translates into hypercompetition for rewarding outcomes. Here the authors show, with empirical analysis and an ecological model, that actors-memes ecosystems evolve towards a narrow set of emergent, natural network patterns. [ABSTRACT FROM AUTHOR]

Mutualistic networks are formed when the interactions between two classes of species are mutually beneficial. They are important examples of cooperation shaped by evolution. Mutualism between animals and plants has a key role in the organization of ecological communities. Such networks in ecology have generally evolved a nested architecture independent of species composition and latitude; specialist species, with only few mutualistic links, tend to interact with a proper subset of the many mutualistic partners of any of the generalist species. Despite sustained efforts to explain observed network structure on the basis of community-level stability or persistence, such correlative studies have reached minimal consensus. Here we show that nested interaction networks could emerge as a consequence of an optimization principle aimed at maximizing the species abundance in mutualistic communities. Using analytical and numerical approaches, we show that because of the mutualistic interactions, an increase in abundance of a given species results in a corresponding increase in the total number of individuals in the community, and also an increase in the nestedness of the interaction matrix. Indeed, the species abundances and the nestedness of the interaction matrix are correlated by a factor that depends on the strength of the mutualistic interactions. Nestedness and the observed spontaneous emergence of generalist and specialist species occur for several dynamical implementations of the variational principle under stationary conditions. Optimized networks, although remaining stable, tend to be less resilient than their counterparts with randomly assigned interactions. In particular, we show analytically that the abundance of the rarest species is linked directly to the resilience of the community. Our work provides a unifying framework for studying the emergent structural and dynamical properties of ecological mutualistic networks. [ABSTRACT FROM AUTHOR]

Understanding the relationship between large-scale structural and functional brain networks remains a crucial issue in modern neuroscience. Recently, there has been growing interest in investigating the role of homeostatic plasticity mechanisms, across different spatiotemporal scales, in regulating network activity and brain functioning against a wide range of environmental conditions and brain states (e.g., during learning, development, ageing, neurological diseases). In the present study, we investigate how the inclusion of homeostatic plasticity in a stochastic whole-brain model, implemented as a normalization of the incoming node’s excitatory input, affects the macroscopic activity during rest and the formation of functional networks. Importantly, we address the structure-function relationship both at the group and individual-based levels. In this work, we show that normalization of the node’s excitatory input improves the correspondence between simulated neural patterns of the model and various brain functional data. Indeed, we find that the best match is achieved when the model control parameter is in its critical value and that normalization minimizes both the variability of the critical points and neuronal activity patterns among subjects. Therefore, our results suggest that the inclusion of homeostatic principles lead to more realistic brain activity consistent with the hallmarks of criticality. Our theoretical framework open new perspectives in personalized brain modeling with potential applications to investigate the deviation from criticality due to structural lesions (e.g. stroke) or brain disorders. [ABSTRACT FROM AUTHOR]

This corrects the article DOI: 10.1038/ncomms14389 [ABSTRACT FROM AUTHOR]