Dietary plant lectins and Parkinson’s disease: A narrative review of gut-brain axis disruption and neuroinflammation

Parkinson’s disease (PD) is a progressive neurodegenerative disorder with multifactorial origins, increasingly linked to gut-derived triggers and environmental factors. Among these, dietary plant lectins — a class of indigestible carbohydrate-binding proteins found in legumes, nightshades, grains, and sprouts have attracted attention for their potential neurotoxic effects. Lectins are known to resist digestion, disrupt intestinal tight junctions, provoke systemic inflammation, and bind to toll-like receptors, mimicking pathogen-associated molecular patterns. These properties may compromise the gut barrier, alter microbiota composition, and activate the immune system, thus contributing to the gut-brain axis disturbances implicated in PD. Some lectins have demonstrated direct neurotoxicity in experimental models by inducing oxidative stress, mitochondrial dysfunction, and dopaminergic neuron apoptosis. Additionally, lectin exposure may promote α-synuclein aggregation and propagation from the enteric nervous system to the brain. This review critically examines current evidence linking dietary lectins to PD pathogenesis, highlighting mechanistic insights and experimental findings. While clinical data remain limited, the biological plausibility supports further investigation into lectins as modifiable dietary factors in neurodegeneration. Future studies should focus on human dietary exposure, gut permeability, and gene–environment interactions to assess their relevance in PD onset and progression. Understanding lectin-related mechanisms may offer novel dietary intervention strategies for PD prevention or management.