Modeling Alzheimer’s progression: Oscillator dynamics on evolving networks #

Christoffer Gretarsson Alexandersen, Alain Goriely, Christian Bick, Willem de Haan

10:30 Tuesday in 2Q50/51.

Part of the Neurodynamics session.

Abstract #

Alzheimer’s disease is the most common cause of dementia and is linked to the spreading of amyloid-β and tau proteins throughout the brain. Recent studies have highlighted stark differences in how amyloid-β and tau affect neurons at the cellular scale. On a larger scale, Alzheimer’s patients are observed to undergo a period of early-stage neuronal hyperactivation followed by deactivation and frequency-slowing of neuronal oscillations. Herein, we model the spreading of both amyloid-β and tau across a human connectome (brain network) and investigate how neuronal dynamics are affected by disease progression. By including the effects of both amyloid-β and tau pathology, our model explains AD-related frequency slowing, early-stage hyperactivation, and late-stage hypoactivation. Investigating the phase-reduction of a minimal model, we show that hyperactivation and frequency-slowing are not due to the topological interactions between regions but are primarily the result of local neurotoxicity.