Role of Sulforaphane in Neurodegenerative Diseases: A Focus on Parkinson’s Disease

Three hallmarks of Parkinson's disease are dopaminergic neuron degeneration, oxidative stress, neuroinflammation, and α-synuclein aggregation. Despite the available therapeutic strategies, they only offer symptomatic relief and do not halt disease progression, and therefore address the need for neuroprotective interventions. The bioactive compound from cruciferous vegetables, sulforaphane has attracted interest for its strong properties as an antioxidant, anti-inflammatory, and detoxification. SFN regulates the Nrf2 pathway, dampens NF-κB signaling, regulates autophagy, and decreases oxidative stress to confer multifaceted neuroprotection. The potential of SFN in the mitigation of PD pathophysiology through mechanistic approaches of inhibiting dopaminergic neuron loss, α-synuclein aggregation, and blood-brain barrier integrity are explored in this review. We also describe SFN’s other major function in other neurodegenerative diseases including Alzheimer’s, Huntington’s, and amyotrophic lateral sclerosis, as comparative insight into broader therapeutic relevance. Because of promising preclinical findings, clinical translation of SFN will require addressing SFN bioavailability issues, stability, and dosing, among others. New approaches to SFN, such as nanoformulations, synergistic combinations, and precision nutrition are presented as new opportunities to improve efficacy in treating PD. Finally, SFN is suggested to be a promising nutraceutical with high neuroprotection potential against PD. Ultimately, work is needed to overcome these translational barriers and determine its role in clinical neurotherapeutics.