The core pathological feature of Parkinson's Disease (PD) is the abnormal aggregation of α-synuclein and the resulting neuronal damage. α-Synuclein exhibits toxic effects when it forms oligomers or fibrils, leading to neuronal death through multiple pathways, including mitochondrial dysfunction, impaired vesicular trafficking, dopamine auto-oxidation, and neuroinflammation. Additionally, α-synuclein can propagate between cells via exosomes, endocytosis/exocytosis, tunneling nanotubes (TNTs), or vagal nerve axonal transport, creating a cascade of pathological effects. This article systematically reviews the structure and function of α-synuclein, its mechanisms of toxicity, intercellular propagation pathways, animal models of overexpression, and potential therapeutic targets based on its pathogenic mechanisms.