Oxidative stress-A direct bridge to central nervous system homeostatic dysfunction and Alzheimer's disease

Neurologists have highly observed a frequent increasing number of elderly patients with Alzheimer's disease (AD) without any relevant evidence of any genetic or known AD-linked predisposing factors in the past few years. Those patients are characterized by continuous and irreversible neuron cells loss along with declined cognitive functions. Numerous studies have suggested that the exaggerated release of reactive oxygen species (ROS) within the brain may develop late-onset neurodegenerative disorders, especially AD-neuroinflammatory type. However, the central nervous system is vitally linked with whole-brain chemical integrity and its related healthy state, the cascade by which ROS may result in AD's development has not been highly justified or even maintained. It is widely known that the brain consumes a vast amount of oxygen and is characterized by being rich in lipid polyunsaturated fatty acids content, explaining why it is a prone region to oxidative stress (OS) and ROS damage. The formed OS-AD cytoskeletal protein aggregates can be considered a main predisposing factor for amyloid-beta (A beta) hallmarks precipitation. Herein, this review aims to provide a detailed information on how oxidative stress can play a pathogenic role in activating damage-associated molecular patterns (DAMPs)-related toll-like receptor-4 inflammatory (TLR-4) cascades resulting in the deposition of A beta hallmarks in brain tissues ending with irreversible cognitive dysfunction. It also explains how microglia can be activated via ROS, which may significantly release several pro-inflammatory cascades ending with general brain atrophy. Furthermore, different types of suggested antioxidant therapies will be discussed to combat AD-related pathological disorders and hallmarks.