The multiphysics of prion-like diseases: progression and atrophy

TL;DR

This paper presents a comprehensive simulation model of toxic protein propagation and brain tissue atrophy in neurodegenerative diseases, reproducing disease progression patterns and linking protein accumulation to tissue degeneration.

Contribution

It introduces a novel coupled transport and mechanical atrophy model that replicates characteristic disease evolution and atrophy patterns in prion-like neurodegenerative diseases.

Findings

Reproduces disease-specific progression patterns

Simulates total toxic protein load evolution

Links protein propagation to tissue atrophy

Abstract

Many neurodegenerative diseases are related to the propagation and accumulation of toxic proteins throughout the brain. The lesions created by aggregates of these toxic proteins further lead to cell death and accelerated tissue atrophy. A striking feature of some of these diseases is their characteristic pattern and evolution, leading to well-codified disease stages visible to neuropathology and associated with various cognitive deficits and pathologies. Here, we simulate the anisotropic propagation and accumulation of toxic proteins in full brain geometry. We show that the same model with different initial seeding zones reproduces the characteristic evolution of different prion-like diseases. We also recover the expected evolution of the total toxic protein load. Finally, we couple our transport model to a mechanical atrophy model to obtain the typical degeneration patterns found in neurodegenerative diseases.