The dismantling of complex networks due to targeted attacks has been extensively studied in network science. A method to assess the centrality of nodes to prioritize the targets of a network attack, namely Network Entanglement (NE), has been introduced in 2021, and a variation accounting for functional effects has been later introduced. The method is based on the concept of network density matrix, inspired by quantum information theory, which has been further developed in the last years.

Complex network states are characterized by the interplay between system’s structure and dynamics. One way to represent such states is by means of network density matrices, whose von Neumann entropy characterizes the number of distinct microstates compatible with given topology and dynamical evolution. In this Letter, we propose a maximum entropy principle to characterize network states for systems with heterogeneous, generally correlated, connectivity patterns and non-trivial dynamics. We focus on three distinct coalescence processes, widely encountered in the analysis of empirical interconnected systems, and characterize their entropy and transitions between distinct dynamical regimes across distinct temporal scales. Our framework allows one to study the statistical physics of systems that aggregate, such as in transportation infrastructures serving the same geographic area, or correlate, such as inter-brain synchrony arising in organisms that socially interact, and active matter that swarm or synchronize.

Complex systems must respond to external perturbations and, at the same time, internally distribute information to coordinate their components. Although networked backbones help with the latter, they limit the components’ individual degrees of freedom and reduce their collective dynamical range. Here we show that real-world networks balance the loss of response diversity with gain in information flow. Encoding network states as density matrices, we demonstrate that such a trade-off mathematically resembles the thermodynamic efficiency characterized by heat and work in physical systems, providing a variational principle to macroscopically explain the sparsity and empirical scaling law observed in hundreds of real-world networks across multiple domains, both analytically and numerically. We show that the emergence of topological features such as modularity, small-worldness and heterogeneity agrees with maximizing the trade-off between information exchange and response diversity from middle to large temporal scales. Our results suggest that the emergence of some of the most prevalent topological features of real-world networks might have a thermodynamic origin.

The information implicitly represented in the state of physical systems allows for their analysis using analytical techniques from statistical mechanics and information theory. This approach has been successfully applied to complex networks, including biophysical systems such as virus-host protein-protein interactions and whole-brain models in health and disease, drawing inspiration from quantum statistical physics. Here we propose a general mathematical framework for modeling information dynamics on complex networks, where the internal node states are vector valued, allowing each node to carry multiple types of information. This setup is relevant for various biophysical and sociotechnological models of complex systems, ranging from viral dynamics on networks to models of opinion dynamics and social contagion. Instead of focusing on node-node interactions, we shift our attention to the flow of information between network configurations. We uncover fundamental differences between widely used spin models on networks, such as voter and kinetic dynamics, which cannot be detected through classical node-based analysis. We illustrate the mathematical framework further through an exemplary application to epidemic spreading on a low-dimensional network. Our model provides an opportunity to adapt powerful analytical methods from quantum many-body systems to study the interplay between structure and dynamics in interconnected systems.

The network density matrix formalism allows for describing the dynamics of information on top of complex structures and it has been successfully used to analyze, e.g., a system's robustness, perturbations, coarse-graining multilayer networks, characterization of emergent network states, and performing multiscale analysis. However, this framework is usually limited to diffusion dynamics on undirected networks. Here, to overcome some limitations, we propose an approach to derive density matrices based on dynamical systems and information theory, which allows for encapsulating a much wider range of linear and nonlinear dynamics and richer classes of structure, such as directed and signed ones. We use our framework to study the response to local stochastic perturbations of synthetic and empirical networks, including neural systems consisting of excitatory and inhibitory links and gene-regulatory interactions. Our findings demonstrate that topological complexity does not necessarily lead to functional diversity, i.e., the complex and heterogeneous response to stimuli or perturbations. Instead, functional diversity is a genuine emergent property which cannot be deduced from the knowledge of topological features such as heterogeneity, modularity, the presence of asymmetries, and dynamical properties of a system.

Microscopic structural damage, such as lesions in neural systems or disruptions in urban transportation networks, can impair the dynamics crucial for systems' functionality, such as electrochemical signals or human flows, or any other type of information exchange, respectively, at larger topological scales. Damage is usually modeled by progressive removal of components or connections and, consequently, systems' robustness is assessed in terms of how fast their structure fragments into disconnected subsystems. Yet, this approach fails to capture how damage hinders the propagation of information across scales, since system function can be degraded even in absence of fragmentation—e.g., pathological yet structurally integrated human brain. Here, we probe the response to damage of dynamical processes on the top of complex networks, to study how such an information flow is affected. We find that removal of nodes central for network connectivity might have insignificant effects, challenging the traditional assumption that structural metrics alone are sufficient to gain insights about how complex systems operate. Using a damaging protocol explicitly accounting for flow dynamics, we analyze synthetic and empirical systems, from biological to infrastructural ones, and show that it is possible to drive the system towards functional fragmentation before full structural disintegration.

Complex biological systems consist of large numbers of interconnected units, characterized by emergent properties such as collective computation. In spite of all the progress in the last decade, we still lack a deep understanding of how these properties arise from the coupling between the structure and dynamics. Here, we introduce the multiscale emergent functional state, which can be represented as a network where links encode the flow exchange between the nodes, calculated using diffusion processes on top of the network. We analyze the emergent functional state to study the distribution of the flow among components of 92 fungal networks, identifying their functional modules at different scales and, more importantly, demonstrating the importance of functional modules for information content of networks, quantified in terms of network spectral entropy. Our results suggest that the topological complexity of fungal networks guarantees the existence of functional modules at different scales keeping the information entropy, and functional diversity, high.

Information exchange in the human brain is crucial for vital tasks and to drive diseases. Neuroimaging techniques allow for the indirect measurement of information flows among brain areas and, consequently, for reconstructing connectomes analyzed through the lens of network science. However, standard analyses usually focus on a small set of network indicators and their joint probability distribution. Here, we propose an information-theoretic approach for the analysis of synthetic brain networks (based on generative models) and empirical brain networks, and to assess connectome's information capacity at different stages of dementia. Remarkably, our framework accounts for the whole network state, overcoming limitations due to limited sets of descriptors, and is used to probe human connectomes at different scales. We find that the spectral entropy of empirical data lies between two generative models, indicating an interpolation between modular and geometry-driven structural features. In fact, we show that the mesoscale is suitable for characterizing the differences between brain networks and their generative models. Finally, from the analysis of connectomes obtained from healthy and unhealthy subjects, we demonstrate that significant differences between healthy individuals and the ones affected by Alzheimer’s disease arise at the microscale (max. posterior probability smaller than 1%) and at the mesoscale (max. posterior probability smaller than 10%).

Complex systems are large collections of entities that organize themselves into non-trivial structures, represented as networks. One of their key emergent properties is robustness against random failures or targeted attacks —i.e., the networks maintain their integrity under removal of nodes or links. Here, we introduce network entanglement to study network robustness through a multiscale lens, encoded by the time required for information diffusion through the system. Our measure’s foundation lies upon a recently developed statistical field theory for information dynamics within interconnected systems. We show that at the smallest temporal scales, the node-network entanglement reduces to degree, whereas at extremely large scales, it measures the direct role played by each node in keeping the network connected. At the meso-scale, entanglement plays a more important role, measuring the importance of nodes for the transport properties of the system. We use entanglement as a centrality measure capturing the role played by nodes in keeping the overall diversity of the information flow. As an application, we study the disintegration of empirical social, biological and transportation systems, showing that the nodes central for information dynamics are also responsible for keeping the network integrated.

Protein–protein interaction networks have been used to investigate the influence of SARS-CoV-2 viral proteins on the function of human cells, laying out a deeper understanding of COVID–19 and providing ground for applications, such as drug repurposing. Characterizing molecular (dis)similarities between SARS-CoV-2 and other viral agents allows one to exploit existing information about the alteration of key biological processes due to known viruses for predicting the potential effects of this new virus. Here, we compare the novel coronavirus network against 92 known viruses, from the perspective of statistical physics and computational biology. We show that regulatory spreading patterns, physical features and enriched biological pathways in targeted proteins lead, overall, to meaningful clusters of viruses which, across scales, provide complementary perspectives to better characterize SARS-CoV-2 and its effects on humans. Our results indicate that the virus responsible for COVID–19 exhibits expected similarities, such as to Influenza A and Human Respiratory Syncytial viruses, and unexpected ones with different infection types and from distant viral families, like HIV1 and Human Herpes virus. Taken together, our findings indicate that COVID–19 is a systemic disease with potential effects on the function of multiple organs and human body sub-systems.

Units of complex systems -- such as neurons in the brain or individuals in societies -- must communicate efficiently to function properly: e.g., allowing electrochemical signals to travel quickly among functionally connected neuronal areas in the human brain, or allowing for fast navigation of humans and goods in complex transportation landscapes. The coexistence of different types of relationships among the units, entailing a multilayer represention in which types are considered as networks encoded by layers, plays an important role in the quality of information exchange among them. While altering the structure of such systems -- e.g., by physically adding (or removing) units, connections or layers -- might be costly, coupling the dynamics of subset(s) of layers in a way that reduces the number of redundant diffusion pathways across the multilayer system, can potentially accelerate the overall information flow. To this aim, we introduce a framework for functional reducibility which allow us to enhance transport phenomena in multilayer systems by coupling layers together with respect to dynamics rather than structure. Mathematically, the optimal configuration is obtained by maximizing the deviation of system's entropy from the limit of free and non-interacting layers. Our results provide a transparent procedure to reduce diffusion time and optimize non-compact search processes in empirical multilayer systems, without the cost of altering the underlying structure.

Any physical system can be viewed from the perspective that information is implicitly represented in its state. However, the quantification of this information when it comes to complex networks has remained largely elusive. In this work, we use techniques inspired by quantum statistical mechanics to define an entropy measure for complex networks and to develop a set of information-theoretic tools, based on network spectral properties, such as Renyi q-entropy, generalized Kullback-Leibler and Jensen-Shannon divergences, the latter allowing us to define a natural distance measure between complex networks. First we show that by minimizing the Kullback-Leibler divergence between an observed network and a parametric network model, inference of model parameter(s) by means of maximum-likelihood estimation can be achieved and model selection can be performed appropriate information criteria. Second, we show that the information-theoretic metric quantifies the distance between pairs of networks and we can use it, for instance, to cluster the layers of a multilayer system. By applying this framework to networks corresponding to sites of the human microbiome, we perform hierarchical cluster analysis and recover with high accuracy existing community-based associations. Our results imply that spectral based statistical inference in complex networks results in demonstrably superior performance as well as a conceptual backbone, filling a gap towards a network information theory.