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Oxidative stress (OS), a condition that occurs when the balance between reactive oxygen species production and antioxidant defense mechanisms is disrupted, has been implicated in the pathogenesis of several neurological conditions, including neurodegenerative and vascular disorders. Ferroptosis is a mechanism mediating OS-induced damage, with growing evidence of specific involvement in both Parkinson's disease (PD) and ischemic stroke. Regular physical activity may have an antioxidant effect by increasing the production and activity of nonenzymatic and enzymatic antioxidants. Among the biological mediators of physical activity, irisin may act as an agent capable of inducing systemic changes and crossing the brain-blood barrier. This review aims to describe the main role of OS in the pathophysiology of PD, highlighting putative neurodegenerative mechanisms and emphasizing the potential targeting by physical activity as a possible shared preventive and symptomatic treatment approach.
Caproni et al. (Wed,) studied this question.