Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder caused by the depletion of dopaminergic neurons in the basal ganglia, the movement center of the brain. Approximately 60,000 people are diagnosed with PD in the United States each year. Although the direct cause of PD can vary, accumulation of oxidative stress-induced neuronal damage due to increased production of reactive oxygen species (ROS) or impaired intracellular antioxidant defenses invariably occurs at the cellular levels. Pharmaceuticals such as dopaminergic prodrugs and agonists can alleviate some of the symptoms of PD. Currently, however, there is no treatment to halt the progression of PD pathology. Due to the nature of PD, a long and progressive neurodegenerative process, strategies to prevent or delay PD pathology may be well suited to lifestyle changes like dietary modification with antioxidant-rich foods to improve intracellular redox homeostasis. In this review, we discuss cellular and genetic factors that increase oxidative stress in PD. We also discuss neuroprotective roles of dietary antioxidants including vitamin C, vitamin E, carotenoids, selenium, and polyphenols along with their potential mechanisms to alleviate PD pathology.
Highlights
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by inadequate levels of dopamine that is caused by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the basal ganglia
Epidemiological studies examining dietary intake of antioxidant micronutrients and the risk of developing PD have yielded equivocal results, and there is a paucity of data from randomized controlled trials among people with pre-existing PD
Vitamin C, vitamin E, and polyphenols directly interact with reactive oxygen species (ROS) and terminate oxidative chain reactions
Summary
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by inadequate levels of dopamine that is caused by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the basal ganglia. Complex I is vulnerable to oxidative damage, and its inhibition is strongly associated with the generation of ROS such as superoxide and hydrogen peroxide presenting a positive feedback loop [8,9,10]. Imbalances in dopamine metabolism contribute to ROS generation, damaging dopaminergic neurons. ROS production and and impairing cellular antioxidant defense systems. Oxidative stressstress damages production impairing cellular antioxidant defense systems. Mitochondrial primes apoptosis, calcium release, andand opening of mtPTP neuritogenesis. Mitochondrialdysfunction dysfunction primes apoptosis, calcium release, opening of mtPTP which leads to the death of neurons, including the specific dopaminergic population of the SNpc which leads to the death of neurons, including the specific dopaminergic population of the SNpc which which produces the and signssymptoms and symptoms.
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