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In widely used models of biological contagion, interventions that randomly rewire edges (generally making them 'longer') accelerate spread. However, recent work has argued that highly clustered, rather than random, networks facilitate the spread of threshold-based contagions, such as those motivated by myopic best response for adoption of new innovations, norms and products in games of strategic complement. Here we show that minor modifications to this model reverse this result, thereby harmonizing qualitative facts about how network structure affects contagion. We analyse the rate of spread over circular lattices with rewired edges and show that having a small probability of adoption below the threshold probability is enough to ensure that random rewiring accelerates the spread of a noisy threshold-based contagion. This conclusion is verified in simulations of empirical networks and remains valid with partial but frequent enough rewiring and when adoption decisions are reversible but infrequently so, as well as in high-dimensional lattice structures. 

Abstract We study Langevin dynamics for recovering the planted signal in the spiked matrix model. We provide a ‘path-wise’ characterization of the overlap between the output of the Langevin algorithm and the planted signal. This overlap is characterized in terms of a self-consistent system of integro-differential equations, usually referred to as the Crisanti–Horner–Sommers–Cugliandolo–Kurchan equations in the spin glass literature. As a second contribution, we derive an explicit formula for the limiting overlap in terms of the signal-to-noise ratio and the injected noise in the diffusion. This uncovers a sharp phase transition—in one regime, the limiting overlap is strictly positive, while in the other, the injected noise overcomes the signal, and the limiting overlap is zero.