Research Article Open Access

A concise overview of the role played by Reactive Oxygen Species in Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is a typical slow progressive neurodegenerative disease that causes dementia in the elderly. Alzheimer’s pace of occurrence is rising in an alarming rate. This disease is categorized as irreversible, debilitating and is distinguishable by the gradual decline of the memory and other cognitive functions as it passes through various stages and ultimately resulting in complete incapacity. It poses a great burden on both the patient and their care takers. The two pathological trademarks of this neurodegenerative disease are aggregated beta-amyloid deposits and hyper phosphorylated neurofibrillary tangles. These lesions are capable of inducing the neuronal damage that eventually leads to cell death associated with a decline in cognitive impairments, through the evolution of reactive oxygen species (ROS). Evidences indicate that the most critical role is of A𝛽 metabolism in prompting the oxidative stress that has been observed in AD patients. The brain retains high levels of ascorbic acid (AA) despite a concentration gradient favouring diffusion from brain to plasma. Age-linked neurological disorders such as Alzheimer’s have long been associated with free radical-induced oxidative stress and these are driven by the no homeostatic generation of reactive oxygen species (ROS). This review particularly examines the possibility of oxidative stress, defined as an imbalance between the formation and quenching of free radicals from oxygen species causing a deleterious condition as the brain cells create more ROS than they can cope up with and this is a major cause of brain cell death.

Sreejani Bandopadhyay

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