Oxidative Stress: The Old Enemy in Alzheimers Disease Pathophysiology

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

Journal Name: Current Alzheimer Research

Volume 2 , Issue 4 , 2005

Become EABM
Become Reviewer
Call for Editor


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.

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

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2005
Page: [403 - 408]
Pages: 6
DOI: 10.2174/156720505774330537
Price: $65

Article Metrics

PDF: 4