On the sufficiency of pairwise interactions in maximum entropy models of networks

DOI10.1007/S10955-016-1456-5zbMATHOpenAlexMaRDI QIDQ290485FDO

Authors Lina Merchan, Ilya Nemenman

Publication date 1 June 2016

Published in Journal of Statistical Physics (Search for Journal in Brave)

Full work available at URL https://arxiv.org/abs/1505.02831

zbMATH Keywords

collective dynamicsnumerical simulations\(p\)-spin models

Mathematics Subject Classification ID

Biochemistry, molecular biology (92C40) Systems biology, networks (92C42) Lattice systems (Ising, dimer, Potts, etc.) and systems on graphs arising in equilibrium statistical mechanics (82B20)

Abstract: Biological information processing networks consist of many components, which are coupled by an even larger number of complex multivariate interactions. However, analyses of data sets from fields as diverse as neuroscience, molecular biology, and behavior have reported that observed statistics of states of some biological networks can be approximated well by maximum entropy models with only pairwise interactions among the components. Based on simulations of random Ising spin networks with $p$-spin ($p>2$) interactions, here we argue that this reduction in complexity can be thought of as a natural property of densely interacting networks in certain regimes, and not necessarily as a special property of living systems. By connecting our analysis to the theory of random constraint satisfaction problems, we suggest a reason for why some biological systems may operate in this regime.

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Cites work

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Cited in

(6)

• A note on asymptotic distributions in maximum entropy models for networks
• Evolution of biomedical innovation quantified via billions of distinct article-level MeSH keyword combinations
• A dynamical state underlying the second order maximum entropy principle in neuronal networks
• Gene coexpression as Hebbian learning in prokaryotic genomes
• Message-passing on hypergraphs: detectability, phase transitions and higher-order information
• Intrachromosomal regulation decay in breast cancer

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