The Possible Impact of Montelukast in Parkinson’s Disease: A Substantial Contribution

Abstract

Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by α-synuclein aggregation and dopaminergic neuron degeneration in the substantia nigra. Evidence suggests that the leukotriene (LT) pathway contributes to PD progression through oxidative stress and neuroinflammatory mechanisms. Purpose: To evaluate the efficacy and neuroprotective potential of the leukotriene receptor antagonist montelukast in the management of PD. Research Design: A narrative review synthesizing evidence from preclinical and clinical studies investigating the effects of montelukast on PD-related neuropathology. Study Sample: Studies indexed in Scopus, Cochrane, Embase, PubMed, and CENTRAL that examined the role of montelukast in PD models or populations. Data Collection and/or Analysis: Two independent reviewers conducted database searches, screened studies for relevance, and extracted data on montelukast’s effects on neuroinflammation, oxidative stress, mitochondrial function, and autophagy. Results: The reviewed evidence indicates that montelukast exhibits neuroprotective activities, including attenuation of neuroinflammation, reduction of oxidative stress, improvement of mitochondrial dysfunction, and enhancement of autophagic processes. These mechanisms collectively contribute to slowing the onset and progression of PD-related neuropathology. Conclusions: Montelukast may offer therapeutic benefits in PD by modulating key pathological processes such as inflammatory signaling, oxidative damage, mitochondrial impairment, and autophagy dysregulation. Further clinical studies are warranted to validate its potential as an adjunct or novel therapeutic option.