Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Increasing evidence suggests that neuroinflammation and oxidative stress play central roles in the pathogenesis and progression of the disease. Chronic activation of microglia, elevated production of pro-inflammatory cytokines, mitochondrial dysfunction, and excessive reactive oxygen species (ROS) contribute to neuronal damage and alpha-synuclein aggregation. This article reviews the molecular mechanisms linking neuroinflammation and oxidative stress in Parkinson’s disease and discusses their potential as therapeutic targets. Understanding these interconnected pathways may provide new opportunities for disease-modifying strategies.