Abstract
Parkinson’s disease (PD) is the second most common neurodegenerative disease and is characterized by dopaminergic neuronal loss. The exact pathogenesis of PD is complex and not yet completely understood, but research has established the critical role mitochondrial dysfunction plays in the development of PD. As the main producer of cytosolic reactive oxygen species (ROS), mitochondria are particularly susceptible to oxidative stress once an imbalance between ROS generation and the organelle’s antioxidative system occurs. An overabundance of ROS in the mitochondria can lead to mitochondrial dysfunction and further vicious cycles. Once enough damage accumulates, the cell may undergo mitochondria-dependent apoptosis or necrosis, resulting in the neuronal loss of PD. Polyphenols are a group of natural compounds that have been shown to offer protection against various diseases, including PD. Among these, the plant-derived polyphenol, resveratrol, exhibits neuroprotective effects through its antioxidative capabilities and provides mitochondria protection. Resveratrol also modulates crucial genes involved in antioxidative enzymes regulation, mitochondrial dynamics, and cellular survival. Additionally, resveratrol offers neuroprotective effects by upregulating mitophagy through multiple pathways, including SIRT-1 and AMPK/ERK pathways. This compound may provide potential neuroprotective effects, and more clinical research is needed to establish the efficacy of resveratrol in clinical settings.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disease afterAlzheimer’s disease (AD) [1]
Other possible mechanisms leading to PD pathology include oxidative damage, mitochondrial dysfunction, the accumulation of α-synuclein, calcium (Ca2+ ) imbalance, the disruption of endo-lysosomal function and autophagy, and neuroinflammation [13,14]
Studies have shown that oxidation of NADPH, with its role in antioxidative protection, further drives Mitochondrial permeability transition (MPT), as NADPH can reduce GSH and thioredoxin (TSH), which participate in the removal of H2 O2 by mitochondrial GSH peroxidase (GPX) and thioredoxin peroxidase (TPX), respectively [81,84]
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disease after. Alzheimer’s disease (AD) [1]. Other possible mechanisms leading to PD pathology include oxidative damage, mitochondrial dysfunction, the accumulation of α-synuclein, calcium (Ca2+ ) imbalance, the disruption of endo-lysosomal function and autophagy, and neuroinflammation [13,14]. As damaged macromolecules resulting from oxidative stress accumulate in the mitochondria, the organelle’s function is disrupted [21] This leads to the release of cytochrome c from the mitochondria and the triggering of cell apoptosis, which can be observed in the dopaminergic neuronal death of PD [21]. The. 16569 base pair, double-stranded, circular mtDNA within the matrix consists of 37 genes and codes for 13 polypeptides critical to the OXPHOS complexes, and a full set of protein translation machinery, including 22 mitochondrial tRNA, a 16S rRNA (large ribosomal unit), and a 12S rRNA (small ribosomal unit) [38,39]. Each human mitochondrion typically contains 2–10 copies of mtDNA and up to 1000 copies per cell, but the actual number can vary according to the cell type [40,41]
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