Oxidativestress‐Adirect bridge to central nervous system homeostatic dysfunction and Alzheimer's disease

Abstract

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 (Aβ) 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 Aβ 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.

Assessing the role of primary healthy microglia and gap junction blocker in hindering Alzheimer’s disease neuroinflammatory type: Early approaches for therapeutic intervention

“…This can be achieved by activating the release of anti-inflammatory cytokines as part of a neuromodulatory response. Thus, the release of IL-10 in the brain mainly results in a direct shift from the M1 phenotype to the M2/TH2 phenotype termed alternative shift ( Martinez et al, 2009 ; Anwar, 2021b ). On the other hand, the resting-balanced microglia phenotype (M0) with ramified appearance is the main type of microglia residing in the parenchyma of the healthy brain.…”

Pteris laeta Wall. and Its New Phytochemical, Pterosinsade A, Promote Hippocampal Neurogenesis via Activating the Wnt Signaling Pathway

“…Mounting evidences suggest that the major pathological changes in AD, Aβ deposition, neurofibrillary tangles, and neuronal apoptosis are associated with oxidative stress damage. 32 Although there is debate on whether oxidative stress is a cause or a consequence of AD, it is certain that oxidative stress damage occurs throughout the development of AD. We noted that PW could improve SOD activity, GSH content, and ROS level, as well as reduce MDA content of Aβinduced HT22 cells.…”

The Protective Effects of S-Methyl Methionine Sulfonium Chloride on Brain Tissue Damage in D-Galactosamine-Induced Hepatotoxicity

“…The hippocampus, amygdala, and brain cells are highly sensitive to the harmful effects of oxidative stress-mediated tissue injury. This is because the brain is an organ containing high amounts of lipids and their derivatives and utilizes high total basal oxygen levels and consequently forms ROS (5). When ROS attack the PUFAs of membrane lipids, the abstraction of hydrogen from PUFA gives rise to the formation of carbon-centered lipid radicals, thus rapidly interacting with the O 2 to form lipid peroxyl radicals.…”

“…On the other hand, the structure and function of biomolecules (e.g., nucleic acids, lipids, carbohydrates, and proteins) may easily change when oxidative stress conditions emerge (4). Given that the brain consumes vast amount of oxygen and is characterized by being rich in polyunsaturated fatty acids (PUFAs) content, its regions (especially the hippocampus, amygdala, and Bayrak et al MMSC Protects GalN-induced Oxidative Brain Injury cerebellar cells) are prone to detrimental effects of oxidative stress and ROS damage as well (5). S-methyl methionine sulfonium chloride (MMSC), also known as vitamin U, has a sulfonium group containing derivative of the essential amino acid L-methionine, that the vegetable source is Brassica species such as white cabbage, Brussel sprouts, kohlrabi, and kale (6).…”