Oxidative Stress and Antioxidants in Neurodegenerative Disorders

Abstract

Neurodegenerative disorders constitute a substantial proportion of neurological diseases with significant public health importance. The pathophysiology of neurodegenerative diseases is characterized by a complex interplay of various general and disease-specific factors that lead to the end point of neuronal degeneration and loss, and the eventual clinical manifestations. Oxidative stress is the result of an imbalance between pro-oxidant species and antioxidant systems, characterized by an elevation in the levels of reactive oxygen and reactive nitrogen species, and a reduction in the levels of endogenous antioxidants. Recent studies have increasingly highlighted oxidative stress and associated mitochondrial dysfunction to be important players in the pathophysiologic processes involved in neurodegenerative conditions. In this article, we review the current knowledge of the general effects of oxidative stress on the central nervous system, the different specific routes by which oxidative stress influences the pathophysiologic processes involved in Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis and Huntington’s disease, and how oxidative stress may be therapeutically reversed/mitigated in order to stall the pathological progression of these neurodegenerative disorders to bring about clinical benefits.

Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases

“…High oxygen consumption, almost entirely oxidative phosphorylation, low energy reserves, high concentrations of peroxidizable lipids, and high levels of iron acting as prooxidants all contribute to this vulnerability [ 12 ]. As a result, neuronal cells are extremely vulnerable to metabolic/ischemic damage and the associated oxidative stress [ 13 ]. The macro- and micromolecular changes of neuronal cells ends in neurodegeneration in various neurological disorders, e.g., post-stroke dementia, Alzheimer’s disease (AD), vascular dementia, and others [ 14 ].…”

NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors

“…To maintain homeostasis and neuronal cell function, the human nervous system consumes about 20% of the amount of oxygen used by the body, causing a large production of ROS. As a result, it could be very sensitive to oxidative stress, which in turn plays a central role in neuroinflammation and neurodegenerative diseases, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS). , In this context, the role of NOXs as a source of ROS, especially NOX2, being the main isoform in the brain besides NOX1 and NOX4, has been intensively investigated. − In experimental animals and in humans, the activation of NOX2, whose overexpression in endothelial cells leads to brain oxidative stress and DNA damage, has been associated with aging-related rarefaction of brain capillaries, loss of neurons, and locomotor disorders, all key aspects of neurodegenerative diseases …”

Effect of Orange Peel Extract on Intestinal Absorption of Aspirin Using Everted Sac Technique

“…Dried Orange peel powder (5 g) was boiled in water (100 mL) for 10 min. After cooling, the sample was centrifuged (5000 rpm for 10 min) and the clear solution was recovered in a conical flask, and then rinsed to 100 mL with water [14].…”