Abstract
Iron species can participate in the Fenton or Fenton-like reaction to generate oxidizing species that can cause oxidative damages to biomolecules and induce oxidative stress in the body. Furthermore, iron accumulation and oxidative stress have been shown to associate with the pathological progression of neurodegenerative disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD). In this review, the role of iron species in generating the most deleterious free radical species (ie, hydroxyl radical) and effects of this species in causing oxidative stress in vivo are described. The implications of oxidative stress and the recently recognized cell death pathway (ie, ferroptosis) to AD are addressed. Strategies to combat this neurodegenerative disease, such as iron chelation and antioxidant therapies, and future research directions on this aspect are also discussed.