I am a Senior Research Scientist at ISI Foundation working on topological approaches to complex networks and their underlying geometry, with special attention to the topology of brain structure and dynamics.
PhD in Complex Networks, 2012
Imperial College London
MSc in Theoretical Physics, 2008
University of Pisa
BSc in Physics, 2005
University of Pisa
10.3.21 I’m giving a talk at the “Virtual Seminars in Complexity” series this friday. Details here. [Recorded talk is now available here]
7.3.21 Quite a few news recently! Starting Feb 2021 for a year I’ll be a Guest Scholar at IMT Lucca visiting the NETWORKS Unit there!
18.2.21 Our paper on limits of parallel capacity is finally out on Nature Physics! You can find the paper here, and a little blurb explaining it here.
8.2.21 New paper “Simplicial and Topological Descriptions of Human Brain Dynamics” out on Network Neuroscience!
3.6.20 New BIG review on higher-order interactions out!! You can find it here. A nice intro to the paper is instead given on Iacopo Iacopini’s page here).
The ability to learn new tasks and generalize performance to others is one of the most remarkable characteristics of the human brain and of recent AI systems. The ability to perform multiple tasks simultaneously is also a signature characteristic of large-scale parallel architectures, that is evident in the human brain, and has been exploited effectively more traditional, massively parallel computational architectures. Here, we show that these two characteristics are in tension, reflecting a fundamental tradeoff between interactive parallelism that supports learning and generalization, and independent parallelism that supports processing efficiency through concurrent multitasking. We formally show that, while the maximum number of tasks that can be performed simultaneously grows linearly with network size, under realistic scenarios (e.g. in an unpredictable environment), the expected number that can be performed concurrently grows radically sublinearly with network size. Hence, even modest reliance on shared representation strictly constrains the number of tasks that can be performed simultaneously, implying profound consequences for the development of artificial intelligence that optimally manages the tradeoff between learning and processing, and for un- derstanding the human brain’s remarkably puzzling mix of sequential and parallel capabilities.
Until recently, little attention has been devoted to the higher-order architecture of real complex systems. However, a mounting body of evidence is showing that taking the higher-order structure of these systems into account can greatly enhance our modeling capacities and help us to understand and predict their emerging dynamical behaviors. Here, we present a complete overview of the emerging field of networks beyond pairwise interactions.
Complex networks have been successfully used to describe the spread of diseases in populations of interacting individuals. Conversely, pairwise interactions are often not enough to characterize social contagion processes such as opinion formation or the adoption of novelties, where complex mechanisms of influence and reinforcement are at work. Here we introduce a higher-order model of social contagion in which a social system is represented by a simplicial complex and contagion can occur through interactions in groups of different sizes. Numerical simulations of the model on both empirical and synthetic simplicial complexes highlight the emergence of novel phenomena such as a discontinuous transition induced by higher-order interactions. We show analytically that the transition is discontinuous and that a bistable region appears where healthy and endemic states co-exist. Our results help explain why critical masses are required to initiate social changes and contribute to the understanding of higher-order interactions in complex systems.
Infectious disease outbreaks recapitulate biology: they emerge from the multi-level interaction of hosts, pathogens, and their shared environment. As a result, predicting when, where, and how far diseases will spread requires a complex systems approach to modeling. Recent studies have demonstrated that predicting different components of outbreaks–e.g., the expected number of cases, pace and tempo of cases needing treatment, importation probability etc.–is feasible. Therefore, advancing both the science and practice of disease forecasting now requires testing for the presence of fundamental limits to outbreak prediction. To investigate the question of outbreak prediction, we study the information theoretic limits to forecasting across a broad set of infectious diseases using permutation entropy as a model independent measure of predictability. Studying the predictability of a diverse collection of historical outbreaks–including, gonorrhea, influenza, Zika, measles, polio, whooping cough, and mumps–we identify a fundamental entropy barrier for time series forecasting. However, we find that for most diseases this barrier to prediction is often well beyond the time scale of single outbreaks, implying prediction is likely to succeed. We also find that the forecast horizon varies by disease and demonstrate that both shifting model structures and social network heterogeneity are the most likely mechanisms for the observed differences in predictability across contagions. Our results highlight the importance of moving beyond time series forecasting, by embracing dynamic modeling approaches to prediction and suggest challenges for performing model selection across long disease time series. We further anticipate that our findings will contribute to the rapidly growing field of epidemiological forecasting and may relate more broadly to the predictability of complex adaptive systems.
Many complex systems find a convenient representation in terms of networks: structures made by pairwise interactions (links) of elements (nodes). For many biological and social systems, elementary interactions involve however more than two elements, and simplicial complexes are more adequate to describe such phenomena. Moreover, these interactions often change over time. Here, we propose a framework to model such an evolution: the Simplicial Activity Driven (SAD) model, in which the building block is a simplex of nodes representing a multi-agent interaction. We show analytically and numerically that the use of simplicial structures leads to crucial differences in the outcome of paradigmatic processes modelling disease propagation or social contagion, with respect to the activity-driven (AD) model, a paradigmatic temporal network model involving only binary interactions. In particular, fluctuations in the number of nodes involved in the interactions can affect the outcome of models of simple contagion processes, contrarily to what happens in the AD model. Moreover, social contagion models such as cascading processes present a much richer phenomenology and can become extremely slow when occurring on evolving simplicial complexes.