Abstract
Overwhelming evidence demonstrates that oxidative stress occurs in brains from patients with Alzheimer's Disease (AD). Whether the oxidative stress is secondary to neurodegeneration, or if it underlies the pathology is not clear. The persistence of AD-related abnormalities in oxidative processes in non-neuronal tissues, including cultured cells, infers that an imbalance in production and removal of reactive oxygen species is an inherent property of cells from AD patients. These results suggest that changes in oxidative processes in AD cells could precede and/or cause AD-related neuropathology. Abnormalities in oxidative processes may also cause changes in signal transduction systems such as calcium that occur in cells from AD patients. The ability to manipulate oxidative processes in peripheral tissues, especially cultured cells, from AD patients should facilitate a mechanistic understanding of the changes in oxidative processes in AD brain. The use of peripheral tissues has the potential to identify both state and trait dependent diagnostic markers, which could be used as endpoints for selecting treatments or monitoring therapeutic effectiveness.