Hareram Birla, Tarun Minocha, Gaurav Kumar, Anamika Misra and Sandeep Kumar Singh* Pages 552 - 562 ( 11 )
Alzheimer’s disease (AD) is one of the life-threatening neurodegenerative disorders in the elderly (>60 years) and incurable across the globe to date. AD is caused by the involvement of various genetic, environmental and lifestyle factors that affect neuronal cells to degenerate over the period of time. The oxidative stress is engaged in the pathogenesis of various disorders and its key role is also linked to the etiology of AD. AD is attributed by neuronal loss, abnormal accumulation of Amyloid-β (Aβ) and neurofibrillary tangles (NFTs) with severe memory impairments and other cognitive dysfunctions which lead to the loss of synapses and neuronal death and eventual demise of the individual. Increased production of reactive oxygen species (ROS), loss of mitochondrial function, altered metal homeostasis, aberrant accumulation of senile plaque and mitigated antioxidant defense mechanism all are indulged in the progression of AD. In spite of recent advances in biomedical research, the underlying mechanism of disruption of redox balance and the actual source of oxidative stress is still obscure. This review highlights the generation of ROS through different mechanisms, the role of some important metals in the progression of AD and free radical scavenging by endogenous molecule and supplementation of nutrients in AD.
Alzheimer's disease (AD), oxidative stress, metal toxicity, mitochondrial dysfunction and neurodegeneration, Reactive Oxygen Species (ROS).
Department of Biochemistry, Institute of Science, Banaras Hindu University, Varanasi-221005, Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi-221005, School of Biomedical Engineering, Indian Institute of Technology, Banaras Hindu University, Varanasi-221005, Institute of medical Science, Banaras Hindu University, Varanasi-221005, Centre of Biomedical Research, SGPGI Campus, Lucknow- 226014