Functional topology inference from network events

In this paper we present a novel approach for inferring functional connectivity within a large-scale network from time series of emitted node events. We do so under the following constraints: (a) non-stationarity of the underlying connectivity, (b) sparsity of the time-series of events, and (c) absence of an explicit model describing how events propagate through the network. We develop an inference method whose output is an undirected weighted network, where the weight of an edge between two nodes denotes the probability of these nodes being functionally connected. Two nodes are assumed to be functionally connected if they show significantly more coincident or short-lagged events than randomly picked pairs of nodes with similar levels of activity. We develop a model of time-varying connectivity whose parameters are determined by maximising the model’s predictive power from one time window to the next. We assess the accuracy, efficiency and scalability of our method on a real dataset of network events spanning multiple months

Functional connectivity inference from time-series of events and application to computer networks

Today’s commercial and Internet Service Provider’s networks are large, heterogeneous, fast-evolving and commonly emit millions of events per second. Monitoring, responding to, and predicting incidents is a key challenge for network management operators. This thesis argues that the concept of functional connectivity, widely used in neuroscience and defined in terms of the presence of statistical dependencies between nodes, can unlock informational value about event logs and assist operators in identifying (and even predicting) service outages. However, existing functional connectivity inference methods are not adapted to event data from computer networks. These methods may either require unavailable models of event propagation, be computationally too costly for large networks and/or long recordings, be not adapted to sparse and discrete activity, and/or assume a static network topology. We thus first describe in depth a major commercial network to highlight the challenges faced by network operators and the opportunities offered by thinking in terms of functional connectivities. Next, using a pair of independent Bernoulli processes as reference, we develop a new statistic aimed at measuring coupling strength by quantifying deviation from independence. However, because many statistics will be large by chance, identifying functional edges from the distribution of statistics over every pair of nodes is challenging. Hence, we then develop a method that infers, in specific contexts, the function that associates each statistic to the probability it accounts for the presence of a functional edge. Next, using the previously described statistic, we propose a novel framework to infer a time-varying functional topology from the time-series of emitted events. Applying this paradigm to two major commercial networks, we show that it can reveal a priori unknown groups of devices providing particular services. Finally, we argue that this thesis has implications beyond assisting network monitoring, such as enabling more robust inference of functional connectivity in neuroscience

Model-free reconstruction of neuronal network connectivity from calcium imaging signals

A systematic assessment of global neural network connectivity through direct electrophysiological assays has remained technically unfeasible even in dissociated neuronal cultures. We introduce an improved algorithmic approach based on Transfer Entropy to reconstruct approximations to network structural connectivities from network activity monitored through calcium fluorescence imaging. Based on information theory, our method requires no prior assumptions on the statistics of neuronal firing and neuronal connections. The performance of our algorithm is benchmarked on surrogate time-series of calcium fluorescence generated by the simulated dynamics of a network with known ground-truth topology. We find that the effective network topology revealed by Transfer Entropy depends qualitatively on the time-dependent dynamic state of the network (e.g., bursting or non-bursting). We thus demonstrate how conditioning with respect to the global mean activity improves the performance of our method. [...] Compared to other reconstruction strategies such as cross-correlation or Granger Causality methods, our method based on improved Transfer Entropy is remarkably more accurate. In particular, it provides a good reconstruction of the network clustering coefficient, allowing to discriminate between weakly or strongly clustered topologies, whereas on the other hand an approach based on cross-correlations would invariantly detect artificially high levels of clustering. Finally, we present the applicability of our method to real recordings of in vitro cortical cultures. We demonstrate that these networks are characterized by an elevated level of clustering compared to a random graph (although not extreme) and by a markedly non-local connectivity.Comment: 54 pages, 8 figures (+9 supplementary figures), 1 table; submitted for publicatio

Revealing networks from dynamics: an introduction

What can we learn from the collective dynamics of a complex network about its interaction topology? Taking the perspective from nonlinear dynamics, we briefly review recent progress on how to infer structural connectivity (direct interactions) from accessing the dynamics of the units. Potential applications range from interaction networks in physics, to chemical and metabolic reactions, protein and gene regulatory networks as well as neural circuits in biology and electric power grids or wireless sensor networks in engineering. Moreover, we briefly mention some standard ways of inferring effective or functional connectivity.Comment: Topical review, 48 pages, 7 figure

A Network Coding Approach to Loss Tomography

Network tomography aims at inferring internal network characteristics based on measurements at the edge of the network. In loss tomography, in particular, the characteristic of interest is the loss rate of individual links and multicast and/or unicast end-to-end probes are typically used. Independently, recent advances in network coding have shown that there are advantages from allowing intermediate nodes to process and combine, in addition to just forward, packets. In this paper, we study the problem of loss tomography in networks with network coding capabilities. We design a framework for estimating link loss rates, which leverages network coding capabilities, and we show that it improves several aspects of tomography including the identifiability of links, the trade-off between estimation accuracy and bandwidth efficiency, and the complexity of probe path selection. We discuss the cases of inferring link loss rates in a tree topology and in a general topology. In the latter case, the benefits of our approach are even more pronounced compared to standard techniques, but we also face novel challenges, such as dealing with cycles and multiple paths between sources and receivers. Overall, this work makes the connection between active network tomography and network coding

Deficits in coordinated neuronal activity and network topology are striatal hallmarks in Huntington's disease.

Background. Network alterations underlying neurodegenerative diseases often precede symptoms and functional deficits. Thus, their early identification is central for improved prognosis. In Huntington's disease (HD), the cortico-striatal networks, involved in motor function processing, are the most compromised neural substrate. However, whether the network alterations are intrinsic of the striatum or the cortex is not fully understood. Results In order to identify early HD neural deficits, we characterized neuronal ensemble calcium activity and network topology of HD striatal and cortical cultures. We used large-scale calcium imaging combined with activity-based network inference analysis. We extracted collective activity events and inferred the topology of the neuronal network in cortical and striatal primary cultures from wild-type and R6/1 mouse model of HD. Striatal, but not cortical, HD networks displayed lower activity and a lessened ability to integrate information. GABAA receptor blockade in healthy and HD striatal cultures generated similar coordinated ensemble activity and network topology, highlighting that the excitatory component of striatal system is spared in HD. Conversely, NMDA receptor activation increased individual neuronal activity while coordinated activity became highly variable and undefined. Interestingly, by boosting NMDA activity, we rectified striatal HD network alterations. Conclusions. Overall, our integrative approach highlights striatal defective network integration capacity as a major contributor of basal ganglia dysfunction in HD and suggests that increased excitatory drive may serve as a potential intervention. In addition, our work provides a valuable tool to evaluate in vitro network recovery after treatment intervention in basal ganglia disorders