Abstract
Reactive species, such as those of oxygen, nitrogen, and sulfur, are considered part of normal cellular metabolism and play significant roles that can impact several signaling processes in ways that lead to either cellular sustenance, protection, or damage. Cellular redox processes involve a balance in the production of reactive species (RS) and their removal because redox imbalance may facilitate oxidative damage. Physiologically, redox homeostasis is essential for the maintenance of many cellular processes. RS may serve as signaling molecules or cause oxidative cellular damage depending on the delicate equilibrium between RS production and their efficient removal through the use of enzymatic or nonenzymatic cellular mechanisms. Moreover, accumulating evidence suggests that redox imbalance plays a significant role in the progression of several neurodegenerative diseases. For example, studies have shown that redox imbalance in the brain mediates neurodegeneration and alters normal cytoprotective responses to stress. Therefore, this review describes redox homeostasis in neurodegenerative diseases with a focus on Alzheimer's and Parkinson's disease. A clearer understanding of the redox-regulated processes in neurodegenerative disorders may afford opportunities for newer therapeutic strategies.
Highlights
Neurodegeneration, which is characterized by gradual neuronal and synaptic degradation, glial focal proliferation, neuroinflammation, vascular abnormalities in specific brain regions, and modifications of proteins such as α-synuclein, amyloid-β, and tau proteins [1,2,3], contributes significantly to the global health burden
Oxidative stress arises as a result of an imbalance in the oxidant/antioxidant ratio and can create a hazardous state that contributes to cellular damage due to a disequilibrium in the number of reactive oxygen species (ROS) molecules generated and the level of the antioxidant enzyme system that detoxifies the reactive intermediates in the biological system [10]
Based on the findings reported by Yang et al [135], the resveratrolencapsulated neuronal mitochondria-targeted micelle designed for their study was able to facilitate the delivery of high levels of resveratrol into the brain mitochondria; this efficiently reduced oxidative stress, decreased Aβ plaque formation, and ameliorated tau hyperphosphorylation, neuroinflammation, and declined memory function in an aged Alzheimer’s disease (AD) mice model
Summary
Neurodegeneration, which is characterized by gradual neuronal and synaptic degradation, glial focal proliferation, neuroinflammation, vascular abnormalities in specific brain regions, and modifications of proteins such as α-synuclein, amyloid-β, and tau proteins [1,2,3], contributes significantly to the global health burden. Oxidative Medicine and Cellular Longevity destroys neural mitochondrial defense mechanisms, causes mitochondrial DNA mutations, affects Ca2+ homeostasis, alters membrane permeability, and damages the mitochondrial respiratory chain. These modifications are thought to play a role in the progression of neurodegenerative disorders by mediating or amplifying neuronal dysfunction and causing neurodegeneration [5]. A series of events, such as oxidative stress, protein modification, and mtDNA damage, eventually results in impaired neuronal proteins, further resulting in neuroinflammation and neurological disorders, which manifest as cognitive function loss [8]. Numerous antioxidant therapeutic targets have been identified that can protect neurons against oxidative stress by preventing free radical formation and modulating normal metal homeostasis [7]. We reviewed scientific reports on the pathogenesis and prospects for therapeutically targeting oxidative stress in neurodegenerative diseases, especially Alzheimer’s and Parkinson’s disease
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