Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities

Sbodio, Juan I.; Snyder, Solomon H.; Paul, Bindu D.

doi:10.1089/ars.2017.7321

Cited by 108 publications

(95 citation statements)

References 573 publications

(571 reference statements)

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“…In the cerebral cortex of aged mice, there is a decline in the levels and activities of G6PD and other GSH-regenerating enzymes ( Dukhande et al, 2009 ). Moreover, G6PD appears to be neuroprotective against endogenous ROS in the aged human brain ( Sbodio et al, 2019 ). However, alterations in G6PD levels in the human brain have not been identified.…”

Section: Pentose Phosphate Pathway Impairmentmentioning

confidence: 99%

Metabolic Dysregulation Contributes to the Progression of Alzheimer’s Disease

Wang

et al. 2020

Front. Neurosci.

126

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Alzheimer's disease (AD) is an incurable neurodegenerative disease. Numerous studies have demonstrated a critical role for dysregulated glucose metabolism in its pathogenesis. In this review, we summarize metabolic alterations in aging brain and ADrelated metabolic deficits associated with glucose metabolism dysregulation, glycolysis dysfunction, tricarboxylic acid (TCA) cycle, oxidative phosphorylation (OXPHOS) deficits, and pentose phosphate pathway impairment. Additionally, we discuss recent treatment strategies targeting metabolic defects in AD, including their limitations, in an effort to encourage the development of novel therapeutic strategies.

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Section: Pentose Phosphate Pathway Impairmentmentioning

confidence: 99%

Metabolic Dysregulation Contributes to the Progression of Alzheimer’s Disease

Wang

et al. 2020

Front. Neurosci.

126

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“…As the brain requires high levels of oxygen to function normally, it is known to be a major repository of free radicals and ROS as well as a high-risk area for neurodegeneration [ 15 , 50 , 51 , 52 ]. OS takes place when an imbalance arises between antioxidants and oxidants [ 53 , 54 , 55 ].…”

Section: Oxidative Stressmentioning

confidence: 99%

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Madireddy

2020

Brain Sciences

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The biochemical integrity of the brain is paramount to the function of the central nervous system, and oxidative stress is a key contributor to cerebral biochemical impairment. Oxidative stress, which occurs when an imbalance arises between the production of reactive oxygen species (ROS) and the efficacy of the antioxidant defense mechanism, is believed to play a role in the pathophysiology of various brain disorders. One such disorder, schizophrenia, not only causes lifelong disability but also induces severe emotional distress; however, because of its onset in early adolescence or adulthood and its progressive development, consuming natural antioxidant products may help regulate the pathogenesis of schizophrenia. Therefore, elucidating the functions of ROS and dietary antioxidants in the pathogenesis of schizophrenia could help formulate improved therapeutic strategies for its prevention and treatment. This review focuses specifically on the roles of ROS and oxidative damage in the pathophysiology of schizophrenia, as well as the effects of nutrition, antipsychotic use, cognitive therapies, and quality of life on patients with schizophrenia. By improving our understanding of the effects of various nutrients on schizophrenia, it may become possible to develop nutritional strategies and supplements to treat the disorder, alleviate its symptoms, and facilitate long-term recovery.

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“…Elimination of peroxides: the limited quantity of LPO products formation and reduction is not harmful to the cellular system. Whereas, the abundant accumulation of LPO products makes the serious complication to the biological system via alternating cell signal and functions [116]. Generally, the biological system eliminates the LPO products via the enzymatic mechanism [117,118].…”

Section: Inhibiting Of Lpo Productsmentioning

confidence: 99%

Role of Lipid Peroxidation Process in Neurodegenerative Disorders

Muthuraman¹,

Rishitha²,

Paramakrishnan³

et al. 2020

Lipid Peroxidation Research

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Lipid peroxidation is one of the primary events of the cell injury process. In pathophysiological condition, it is undergoing the initiation of organ damage. Various free radicals are playing a key role in this lipid peroxidation process. Free radical associated organ damage involves the three major phases, that is, initiation, propagation and termination. The primary source of various free radical formations is mediated through the pathophysiological function of mitochondria. Lipid peroxidation is contributed to the multiple neurodegenerative disorders. Thus, the various endogenous cellular anti-oxidant systems are regulated lipid peroxidation process and control the neurodegenerative action. Some of the molecules are targeted to attenuate the lipid peroxidation and their mediators for the prevention of neurodegeneration.

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Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities

Cited by 108 publications

References 573 publications

Metabolic Dysregulation Contributes to the Progression of Alzheimer’s Disease

Metabolic Dysregulation Contributes to the Progression of Alzheimer’s Disease

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Role of Lipid Peroxidation Process in Neurodegenerative Disorders

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