Title:Role of Oxidative Stress and Metal Toxicity in the Progression of Alzheimer’s Disease
VOLUME: 18 ISSUE: 7
Author(s):Hareram Birla, Tarun Minocha, Gaurav Kumar, Anamika Misra and Sandeep Kumar Singh*
Affiliation: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
Keywords:Alzheimer's disease (AD), oxidative stress, metal toxicity, mitochondrial dysfunction and neurodegeneration,
Reactive Oxygen Species (ROS).
Abstract: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.
