A Second Look into the Oxidant Mechanisms in Alzheimers Disease

Title: A Second Look into the Oxidant Mechanisms in Alzheimers Disease

Volume: 2 Issue: 2

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

Affiliation:

Keywords: alzheimer disease, amyloid, oxidative stress, reactive oxygen species, tau

Abstract: Oxidative damage is a major feature of Alzheimers disease pathophysiology. Instead of succumbing to these oxidative abnormalities, neurons upregulate antioxidant defenses, which suggest a novel balance in oxidant homeostasis in Alzheimers disease. Evidence indicates that in the initial phase of Alzheimers disease development, amyloid-β deposition and hyperphosphorylated τ are consequences of oxidative stress and function as a primary line of antioxidant defense. However, during the progression of the disease, the antioxidant activity of both agents evolves into pro-oxidant, representing a typical gain-of-function transformation. This transformation is due to an increase in reactive species and a decrease in clearance mechanisms. However, the notion that amyloid-β and hyperphosphorylated t function as protective components in the early stages of Alzheimers disease brings into serious question the rationale of current therapeutic strategies aimed to remove both amyloid-β and hyperphosphorylated τ.

Cite this article as:

Moreira I. Paula, Oliveira R. Catarina, Santos S. Maria, Nunomura Akihiko, Honda Kazuhiro, Zhu Xiongwei, Smith A. Mark and Perry George, A Second Look into the Oxidant Mechanisms in Alzheimers Disease, Current Neurovascular Research 2005; 2 (2) . https://dx.doi.org/10.2174/1567202053586758