This review reframes Parkinson's disease as a heterogeneous syndrome, synthesizing genetic (SNCA, LRRK2, VPS35, RAB32, PRKN, PINK1, GBA1 and >90 GWAS loci) and neuroinflammatory evidence that converges on pathways like alpha‑synuclein aggregation, lysosomal dysfunction, mitochondrial impairment,…

By integrating genetic and immune mechanisms the paper highlights convergent, actionable biological pathways and patient‑stratification opportunities that can guide disease‑modifying therapeutic discovery and biomarker development.

Parkinson's disease (PD) is increasingly recognised as a multifactorial and heterogeneous condition rather than a single uniform disorder, supported by advances in molecular biology, genetics and pathology. This review provides a perspective on the shifting concept of PD from an idiopathic, strictly defined pathological entity to a highly heterogeneous clinical and etiopathological condition. We outline the diverse aetiologic pathways and clinical expressions of PD, with particular emphasis on genetic contributors and the role of neuroinflammation. Genetic studies have identified monogenic causes - including SNCA, LRRK2, VPS35, RAB32, PRKN and PINK1 - as well as increased risk linked to heterozygous GBA1variants and more than 90 susceptibility loci from genome-wide association studies (GWAS), highlighting converging pathogenic mechanisms. Recent work underscores significant involvement of innate and adaptive immune responses from the earliest disease stages, suggesting a central shared role in PD onset and progression. This contemporary framework opens new avenues for biology-based, disease-modifying therapeutic strategies.