Interplay of antioxidants in Alzheimer’s disease

Abstract

The generation of reactive oxygen species (ROS) results in oxidative stress, leading to damage of tissue via many cellular molecular pathways. ROS can result in damage of principal cellular components of the cell such as lipids, proteins, and nucleic acids which then cause cell death via different modes of necrosis or apoptosis. Therefore, it is very important to maintain the redox status in our body. This is maintained by balance in the production of free radicals and antioxidants. Oxidative stress is the main phenomena which occur in progression of many diseases such as diabetes, neurodegenerative diseases, cancers etc. Alzheimer disease (AD) is one of the neurodegenerative disease and is common form of dementia in elderly people. The etiology of this disease is multifactorial; pathologically it is accompanied with accumulation of amyloid beta and neurofibrillary tangles. Accumulation of amyloid beta and mitochondrial dysfunction leads to oxidative stress. There is natural antioxidant defence system in our body which helps us to prevent us from various diseases via different mechanisms. Antioxidants are believed to act against the detrimental effects of ROS and thereby preventing or treating oxidative stress-related diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) is an emerging regulator of cellular resistance to oxidants. It controls the basal and induced expression of antioxidant response element-dependent genes. The current review examined the extensive role of oxidative stress in AD. Further investigation into the role that oxidative stress mechanisms seem to play in the pathogenesis of Alzheimer disease may lead to novel clinical interventions.