Parkinson’s disease is marked by the progressive loss of dopaminergic neurons and the prion-like spread of misfolded α-synuclein. This study presents a computational framework simulating α-synuclein propagation and neuron death within a simplified substantia nigra model. Cellular automata were used to model local transmission, oxidative stress, and cumulative toxicity, while Braak-stage-informed parameters guided regional progression. The simulation explores how mitochondrial stress thresholds and α-synuclein seeding density alter neurodegeneration patterns. This model provides a visualizable, modular tool to test hypotheses on disease progression and therapeutic timing.
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Mirchandani et al. (2025) studied this question.
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