Neuronal activity induces symmetry breaking in neurodegenerative disease spreading

Abstract

Dynamical systems on networks typically involve several dynamical processes evolving at different timescales. For instance, in Alzheimers disease, the spread of toxic protein throughout the brain not only disrupts neuronal activity but is also influenced by neuronal activity itself, establishing a feed-back loop between the fast neuronal activity and the slow protein spreading. Motivated by the case of Alzheimers disease, we study the multiple-timescale dynamics of a heterodimer spreading process on an adaptive network of Kuramoto oscillators. Using a minimal two-node model, we establish that heterogeneous oscillatory activity facilitates toxic outbreaks and induces symmetry breaking in the spreading patterns. We then extend the model formulation to larger networks and perform numerical simulations of the slow-fast dynamics on common network motifs and on the brain connectome. The simulations corroborate the findings from the minimal model, underscoring the significance of multiple-timescale dynamics in the modeling of neurodegenerative diseases.