Oxidative Stress: The Old Enemy in Alzheimers Disease Pathophysiology

Title: Oxidative Stress: The Old Enemy in Alzheimers Disease Pathophysiology

Volume: 2 Issue: 4

Author(s): Paula I. Moreira, Kazuhiro Honda, Quan Liu, Maria S. Santos, Catarina R. Oliveira, Gjumrakch Aliev, Akihiko Nunomura, Xiongwei Zhu, Mark A. Smith and George Perry

Affiliation:

Keywords: alzheimer disease, amyloid-b, metal, mitochondria, oxidative stress

Abstract: The complex nature and genesis of oxidative damage in Alzheimer disease can be partly answered by mitochondrial and redox-active metal abnormalities. By releasing high levels of hydrogen peroxide, dysfunctional mitochondria propagate a series of interactions between redox-active metals and oxidative response elements. In the initial phase of disease development, amyloid-β deposition and hyperphosphorylated t may function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative injuries. However, during the progression of the disease, the antioxidant activity of both agents evolves into pro-oxidant activity representing a typical gain-offunction transformation, which can result from an increase in reactive species and a decrease in clearance mechanisms.

Cite this article as:

Moreira I. Paula, Honda Kazuhiro, Liu Quan, Santos S. Maria, Oliveira R. Catarina, Aliev Gjumrakch, Nunomura Akihiko, Zhu Xiongwei, Smith A. Mark and Perry George, Oxidative Stress: The Old Enemy in Alzheimers Disease Pathophysiology, Current Alzheimer Research 2005; 2 (4) . https://dx.doi.org/10.2174/156720505774330537