This review explores the "endotoxin hypothesis" of Parkinson's disease (PD), suggesting that elevated levels of lipopolysaccharide (LPS) from gut dysfunction contribute to PD progression. LPS promotes α-synuclein aggregation, microglial activation, neuroinflammation, and dopaminergic neuron loss in the brain. The hypothesis posits that gut-derived LPS and cytokines induce systemic inflammation, which
