Parkinson’s disease (PD) is a progressive neurodegenerative condition characterized by dopaminergic neuronal loss in the substantia nigra, which is accompanied by both genetic and inflammatory causes. Recent studies have highlighted the simultaneous importance of genetic predisposition and neuroinflammatory mechanisms in disease development, progression, and clinical heterogeneity. The present paper intends to review current research on the roles of neuroinflammation and genetic variables in PD etiology, as well as to assess their interplay, diagnostic relevance, and treatment promise. This narrative review brings together data from recent studies on monogenic mutations (e.g., SNCA, LRRK2, GBA1), inflammatory signaling pathways, glial cell dysfunction, experimental models, and biomarker research. Therapeutic developments addressing these processes are also discussed, with a focus on translational progress and new trends. The combination of neuroinflammation and genetics provides significant insights into the disease pathogenesis. A focus is observed on developing biomarkers and precision medicine approaches that target both pathways; this provides hope for an earlier diagnosis and more successful, tailored treatment strategies in the future.
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