Parkinson's disease (PD) is a multifactorial neurodegenerative disorder characterized by dopaminergic neuronal loss and complex pathogenic mechanisms, including oxidative stress, mitochondrial dysfunction, neuroinflammation, protein misfolding, and autophagic impairment. Current therapeutic regimens primarily offer symptomatic relief and lack disease-modifying efficacy. In this study, a network pharmacology framework was employed to elucidate the multi-target mechanisms of demethoxycurcumin, a bioactive curcuminoid derived from the Ayurvedic herb Curcuma longa. Potential protein targets of demethoxycurcumin were predicted through SwissTargetPrediction and mapped against PD-associated genes retrieved from the GeneCards database, yielding 83 overlapping targets. Protein–protein interaction (PPI) network analysis, conducted using STRING and visualized in Cytoscape, identified key hub genes including AKT1, TNF, EP300, APP, EGFR, MTOR, STAT3, NFE2L2, GSK3B, and BRAF. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed significant involvement of these targets in biological processes such as protein phosphorylation, amyloid-β response, and tyrosine kinase signaling, as well as pathways related to neuroinflammation and intracellular signaling. Molecular docking analysis using AutoDock Vina demonstrated a lowest binding affinity of demethoxycurcumin to AKT1 (–7.557 kcal/mol), supported by hydrogen bonding and hydrophobic interactions. Collectively, these findings suggest that demethoxycurcumin may exert neuroprotective effects in PD through modulation of multiple molecular targets and signaling pathways, thus supporting its potential as a multitarget therapeutic candidate for neurodegenerative diseases.