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Uemura, N. and Oka, A. (2021) Pathophysiological Mechanisms of α-Synuclein Spread in Parkinson’s Disease. Neurobiology of Disease, 153, Article 105327.

has been cited by the following article:

• TITLE: Computational Modeling of Dopaminergic Neuron Degeneration and α-Synuclein Spread in Parkinson’s Disease

  AUTHORS: Preeti S. Mirchandani, Vriti Mirchandani

  KEYWORDS: Parkinson’s Disease, α-Synuclein Aggregation, Dopaminergic Neuron Degeneration, Oxidative Stress, Reactive Oxygen Species, Substantia Nigra, Prion-Like Propagation, Braak Staging, Neurodegeneration Modeling, Cellular Automata, Agent-Based Modeling, Computational Neuroscience, Mitochondrial Dysfunction, Antioxidant Therapy, Disease Progression Simulation, Neuronal Vulnerability, Neural Grid Simulation, Early Intervention Modeling, ROS Dynamics, Therapeutic Timing, Neuroinflammation, Parkinson’s Biomarkers

  JOURNAL NAME: Advances in Parkinson's Disease, Vol.14 No.3, July 22, 2025

  ABSTRACT: 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.