Role of oxidative stress in Alzheimer's disease

Abstract

Alzheimer's disease is the leading cause of disability in people over 65. Amyloid (Aβ) peptide deposition, neurofibrillary tangles of hyperphosphorylated protein, and dementia are hallmarks of AD [1]. The neurotoxic oligomer Aβ peptide and tau protein [2] mediate neurodegeneration, one of the main causes of the disease. Oxidative stress [3], an imbalance between antioxidants and oxidants, causes and exacerbates these symptoms. Free radicals, which have one or more unpaired electrons in their outer shell, can augment or reduce antioxidant defence, causing this imbalance. The reduction of molecular oxygen in water produces superoxide, which produces hydrogen peroxide by adding an electron. Reactive oxygen species (ROS) [4]—hydroxyl radicals produced by hydrogen peroxide reduction—can react with lipids, proteins, nucleic acids, and other molecules and change their structures and activities. Due to its makeup, ROS affects tissues and organs, particularly the sensitive brain. High oxygen usage and highly oxidizable lipids make up the brain.